Emergencies in Critical Care [2 ed.] 9780199696277

Table of contents :
Cover
Contents
Contributors
Symbols and abbreviations
1 Assessment and stabilization
2 Airway
3 Breathing
4 Circulation
5 Neurology
6 Metabolic, endocrine, and environmental injury
7 Renal
8 Gastrointestinal and hepatic
9 Haematology and oncology
10 Infections
11 Surgical patients
12 Trauma, burns, and skin injury
13 Obstetric and fertility patients
14 Poisoning and overdose
15 Incidents and adverse events
16 Communication and organ donation
17 Common emergency procedures
Appendix
Index
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
Y
Z

Citation preview

OXFORD MEDICAL PUBLICATIONS

Emergencies in Critical Care

Published and forthcoming titles in the Emergencies in... series: Emergencies in Adult Nursing Edited by Philip Downing Emergencies in Anaesthesia Edited by Keith Allman, Andrew McIndoe, and Iain H. Wilson Emergencies in Cardiology Edited by Saul G. Myerson, Robin P. Choudhury, and Andrew Mitchell Emergencies in Children’s and Young People’s Nursing Edited by E.A. Glasper, Gill McEwing, and Jim Richardson Emergencies in Clinical Surgery Edited by Chris Callaghan, Chris Watson and Andrew Bradley Emergencies in Critical Care, 2e Edited by Martin Beed, Richard Sherman, and Ravi Mahajan Emergencies in Gastroenterology and Hepatology Marcus Harbord and Daniel Marks Emergencies in Mental Health Nursing Edited by Patrick Callaghan Emergencies in Obstetrics and Gynaecology Edited by S. Arulkumaran Emergencies in Oncology Edited by Martin Scott-Brown, Roy A.J. Spence, and Patrick G. Johnston Emergencies in Paediatrics and Neonatology, 2e Edited by Stuart Crisp and Jo Rainbow Emergencies in Palliative and Supportive Care Edited by David Currow and Katherine Clark Emergencies in Primary Care Chantal Simon, Karen O’Reilly, John Buckmaster, and Robin Proctor Emergencies in Psychiatry, 2e Basant Puri and Ian Treasaden Emergencies in Radiology Edited by Richard Graham and Ferdia Gallagher Emergencies in Respiratory Medicine Edited by Robert Parker, Catherine Thomas, and Lesley Bennett Emergencies in Sports Medicine Edited by Julian Redhead and Jonathan Gordon Head, Neck and Dental Emergencies Edited by Mike Perry Medical Emergencies in Dentistry Nigel Robb and Jason Leitch

Emergencies in Critical Care Second edition

Edited by

Martin Beed Consultant in Critical Care and Anaesthesia Nottingham University Hospitals, UK

Richard Sherman Consultant in Critical Care and Anaesthesia Nottingham University Hospitals, UK

Ravi Mahajan Professor and Honorary Consultant in Anaesthesia and Intensive Care Medicine University of Nottingham Nottingham University Hospitals, UK

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Great Clarendon Street, Oxford, OX2 6DP, United Kingdom Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship, and education by publishing worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and in certain other countries © Oxford University Press 2013 The moral rights of the authors have been asserted First Edition published in 2007 Second Edition published in 2013 Impression: 1 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by licence or under terms agreed with the appropriate reprographics rights organization. Enquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above You must not circulate this work in any other form and you must impose this same condition on any acquirer British Library Cataloguing in Publication Data Data available ISBN 978–0–19–969627–7 Printed in China by C&C Offset Printing Co. Ltd Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding. Links to third party websites are provided by Oxford in good faith and for information only. Oxford disclaims any responsibility for the materials contained in any third party website referenced in this work.

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Preface to the second edition This book is intended to be useful to doctors and nurses based on the intensive care unit (ICU) and on the wards, containing the key elements of how to manage critically ill patients in those first few crucial hours. Where possible the book follows an ‘ABC’ format, the commonest approach to dealing with emergencies; and this new edition has been updated to try and make that ‘ABC’ management as simple as possible. Key history and examination findings are listed as often as possible, as are drug doses and investigation results. There is even some deliberate duplication, so that the reader doesn’t have to jump to different parts of the book to get that crucial piece of information. For those based on the ICU or high dependency unit, this book also contains details of how to deal with common conditions that are managed in subtly different ways within a critical care environment; as well as conditions which are peculiar to ICU (e.g. complications associated with mechanical ventilation). Emergencies in critical care are often surprisingly predictable, and the knowledge of who is likely to be at risk, and how they may be best managed, will provide those involved with a rational approach for these stressful situations. Guidelines are reviewed and updated regularly, and wherever possible the latest versions have been included in this new edition. We have also included references to key documents, high-quality review articles, or seminal ICU articles. We have continued to include a broad spectrum of diseases and emergencies, expanding in some areas and simplifying in others, in order to try and present the clearest and most concise summary of all the essential information. The first half of the book describes the management of emergencies affecting various systems, whilst the second half concentrates on various groups of patients or conditions. Most chapters begin with a generic description of how to manage emergencies affecting that system or patient group. This is followed by details of specific diagnoses and how they should be managed. In short we hope that this new edition will prove invaluable to you, no matter what your position, grade, or experience, whenever you are faced with a critically ill patient, either as a guide to management or an aide-memoire for those hard-to-remember facts. M.B. R.S. R.M. March 2013

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Contents Contributors ix Symbols and abbreviations x 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17

Assessment and stabilization Airway Breathing Circulation Neurology Metabolic, endocrine, and environmental injury Renal Gastrointestinal and hepatic Haematology and oncology Infections Surgical patients Trauma, burns, and skin injury Obstetric and fertility patients Poisoning and overdose Incidents and adverse events Communication and organ donation Common emergency procedures Appendix 561 Index 581

1 17 47 97 151 203 255 271 297 321 387 403 425 447 495 505 513

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Contributors Steve Beed

Martin Levitt

Teacher and artist

Consultant in Critical Care and Anaesthesia Nottingham University Hospitals Nottingham, UK

Victoria Banks SpR in Critical Care and Anaesthesia Nottingham University Hospitals Nottingham, UK

Thearina De Beer Consultant in Critical Care and Anaesthesia Nottingham University Hospitals Nottingham, UK

Myles Dowling Consultant in Anaesthesia Nottingham University Hospitals Nottingham, UK

Lewis Gray SpR in Critical Care and Anaesthesia Nottingham University Hospitals Nottingham, UK

Dan Harvey Consultant in Critical Care and Anaesthesia Nottingham University Hospitals Nottingham, UK 1

Mandy Haughton

Senior Staff Nurse Nottingham University Hospitals Nottingham, UK

Lina Hijazi Consultant in Genito-urinary and HIV Medicine Whipps Cross Hospital Barts NHS Trust London, UK 1

Contributors to the first edition only

Gareth Moncaster1 Consultant in Critical Care and Anaesthesia Sherwood Forest Hospitals Nottinghamshire, UK

Matt O’Meara SpR in Critical Care and Anaesthesia Nottingham University Hospitals Nottingham, UK

Rajkumar Rajendrum1 SpR in Anaesthesia and Intensive Care John Radcliffe Hospital Oxford, UK

Andrew Sharman Consultant in Critical Care and Anaesthesia Nottingham University Hospitals Nottingham, UK

Suzanne Wallace Consultant Obstetrician Nottingham University Hospitals Nottingham, UK

Sandy Whitehead1 Senior Staff Nurse Nottingham University Hospitals Nottingham, UK

Jonny Wilkinson Consultant in Critical Care and Anaesthesia Northampton General Hospital Northampton, UK

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Symbols and abbreviations b i d p s M 7 2,3 DPG 5HIAA βHCG A&E A-a AAA ABC ABGs AC ACA ACE ACh AChR ACS ACT ACTH ADH AF AFB AFE AIDS AKI ALI ALL ALP ALS ALT AMPLE history

cross reference increased decreased primary secondary website approximately 2,3-diphosphoglycerate hydroxy-indole acetic acid human chorionic gonadotropin beta-subunit accident and emergency (see also ED) alveolar/arterial [oxygen gradient] abdominal aortic aneurysm airway, breathing, circulation arterial blood gases alternating current anterior cerebral artery angiotensin-converting enzyme acetylcholine acetylcholine receptor abdominal compartment syndrome or acute coronary syndrome activated clotting time adrenocorticotropic hormone anti-diuretic hormone atrial fibrillation acid-fast bacilli amniotic fluid embolism acquired immune deficiency syndrome acute kidney injury acute lung injury acute lymphocytic leukaemia alkaline phosphatase advanced life support alanine aminotransferase Allergies, Medication, Past medical history, Last meal, Environment

SYMBOLS AND ABBREVIATIONS

ANA ANCA AP APACHE (II) APH APP APTT ARB(A)s ARDS ARF ASB ASD AST ATLS ATN AVM AVPU AXR BAL BBB BE BIPAP BIS BLS BM BMI BNF BOS BP BPF BSA Ca2+ CALS CAM-ICU cAMP CAP CAPD CAVH

antinuclear antibodies antinuclear cytoplasmic antibodies antero-posterior [X-rays] acute physiology and chronic health evaluation [score, version II] antepartum haemorrhage abdominal perfusion pressure activated partial thromboplastin time angiotensin receptor blockers (or antagonists) acute respiratory distress syndrome acute renal failure assisted spontaneous breathing atrial septal defect aspartate aminotransferase advanced trauma life support acute tubular necrosis arteriovenous malformation Alert, responds to Voice, responds to Pain, Unresponsive [consciousness assessment] abdominal X-ray broncho-alveolar lavage blood–brain barrier base excess biphasic positive airways pressure bispectral index basic life support bone marrow or blood monitoring [glucose] body mass index British National Formulary base of skull [fracture] blood pressure bronchopleural fistula body surface area calcium cardiac surgery advanced life support confusion assessment method for the ICU cyclic adenosine monophosphate community-acquired pneumonia continuous ambulatory peritoneal dialysis continuous arterio-venous haemofiltration

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SYMBOLS AND ABBREVIATIONS

CCF CCHF CCU CDT CFI CF (A) M CHF CI CIN CIWA-Ar CJD CK CKMB CLL CMV CNS CO CO2 COHb COPD CPAP CPIS CPP CPR CPT CRBSI CRP CRT CSL C-spine CSF CSU CT CT CTG CTPA CURB-65 CVA CVC

congestive cardiac failure Crimean-Congo haemorrhagic fever coronary care unit Clostridium difficile toxin cardiac function index cerebral function (analysing) monitor congestive heart failure cardiac index contrast induced nephropathy Clinical Institute withdrawal assessment of alcohol (revised) scale Creutzfeld–Jakob disease creatine kinase CK myocardial bound [portion] chronic lymphocytic leukaemia cytomegalovirus or continuous mandatory ventilation central nervous system cardiac output or carbon monoxide carbon dioxide carboxyhaemoglobin chronic obstructive pulmonary disease continuous positive airways pressure clinical pulmonary infection score cerebral perfusion pressure cardiopulmonary resuscitation cryoprecipitate catheter-related blood stream infection C-reactive protein capillary refill time compound sodium lactate [fluid] cervical spine cerebrospinal fluid catheter specimen urine lung compliance (thoracic compliance) computed tomography cardiotocograph CT pulmonary angiogram [a pneumonia scoring system] cerebrovascular accident central venous catheter

SYMBOLS AND ABBREVIATIONS

CVP CVS CVVH CXR DAP DC DCI DDT DHI DI DIC DKA DLT DM DMPS DMSA DNAR DO2 DOB DOH DNA DPL DRESS ds-DNA DTs DVT EBV ECCO2R ECG ECHO ECMO ED EDTA EEG EF eGFR EMG ENT ERCP ESR

central venous pressure cardiovascular system continuous veno-venous haemofiltration chest X-ray diastolic aortic pressure direct current delayed cerebral ischaemia dichloro diphenyl tricholoethane dynamic hyperinflation diabetes insipidus disseminated intravascular coagulopathy diabetic ketoacidosis double lumen [ET] tube diabetes mellitus sodium 2,3-dimercapto-1-propane sulphonate dimercaptosuccinic acid do not attempt resuscitation oxygen delivery date of birth department of health deoxyribonucleic acid diagnostic peritoneal lavage drug rash with eosinophilia and systemic symptoms double stranded DNA delirium tremens deep vein thrombosis Epstein–Barr virus extracorporeal carbon dioxide removal electrocardiogram echocardiogram (TOE or TTE) extracorporeal membrane oxygenation emergency department (see also A&E) ethylene diamine tetraacetic acid electroencephalogram ejection fraction estimated glomerular filtration rate electromyograph ear, nose, and throat endoscopic retrograde cholangiopancreatography erythrocyte sedimentation rate

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SYMBOLS AND ABBREVIATIONS

ETCO2 ETT EVLWI EWS FAST FBC FDPs Fe FES FEV1 FiO2 FFP FOB FOI Fr FRC FTc FVC G G&S GBM GBS GCS GEDVI GFR GGT GHB GI(T) GnRH GP GP2b3a GSW GTN GU HAART HAI HAP HAS HAV HAV-IgM

end-tidal carbon dioxide endotracheal tube extravascular lung water index early warning score focused assessment with sonography for trauma full blood count fibrinogen degradation products iron fat embolism syndrome forced expiratory volume in 1 second fraction of inspired O2 fresh frozen plasma faecal occult blood fibreoptic intubation French gauge functional residual capacity corrected flow time forced vital capacity gauge group and save glomerular basement membrane Guillain–Barré syndrome Glasgow coma score global end diastolic volume index glomerular filtration rate gamma-glutamyl transpeptidase gammahydroxybutyric acid gastrointestinal (tract) gonadotrophin releasing hormone general practitioner glycoprotein 2b3a [receptor inhibitor] gunshot wounds glyceryl trinitrate genitourinary highly active antiretroviral therapy hospital-acquired infection hospital-acquired pneumonia human albumin solution hepatitis A virus hepatitis A antibody

SYMBOLS AND ABBREVIATIONS

Hb HbA1C HBcore-IgM HbsAg HBV hCG HCAP Hct HCV HD HELLP HEPA [mask] HFOV HHS HiB HIT (S) HIV HMMA HOCM HONK HPA (CFI) HR HRS HSP HSV HUS IABP IAH IAP IBC IBW ICP ICU ID card IDDM I:E ratio IgE IHD IJ IM

haemoglobin glycosylated haemoglobin hepatitis B core antibody hepatitis B surface antigen hepatitis B virus human chorionic gonadotrophin healthcare-associated pneumonia haematocrit hepatitis C virus haemodialysis haemolysis, elevated liver enzymes, low platelets high-efficiency particulate air high-frequency oscillatory ventilation hyperosmolar hyperglycaemic state Haemophilus influenzae type b heparin-induced thrombocytopaenia (syndrome) human immunodeficiency virus hydroxymethylmandelic acid hypertrophic obstructive cardiomyopathy hyperosmolar non-ketotic [coma] Health Protection Agency (centre for infections) heart rate hepatorenal syndrome Henoch–Schönlein purpura herpes simplex virus haemolytic uraemic syndrome intra-aortic balloon pump intra-abdominal hypertension intra-abdominal pressure iron binding capacity ideal body weight intracranial pressure intensive care unit identification card insulin dependent diabetes mellitus inspired:expired [air] ratio immunoglobulin E ischaemic heart disease internal jugular intramuscular

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SYMBOLS AND ABBREVIATIONS

INR IO IOP IPPV IRIS (or IRS) ITBVI ITP ITU IUFD IV IVC IVIG IVU IVF JVP K+ KCO LACS LAP LBBB LDH LFTs LH LiDCO™ LMA LMWH LP LRTI LSD LV LVAD LVEDP LVF LVSWI MAHA MAOI MAP MARS MBA MCA

international normalized ratio intraosseous intraocular pressure intermittent positive pressure ventilation immune reconstitution inflammatory syndrome intrathoracic blood volume index idiopathic thrombocytopaenic purpura intensive therapy unit intrauterine fetal death intravenous inferior vena cava intravenous immunoglobulin intravenous urogram in vitro fertilization jugular venous pressure potassium transfer coefficient lacunar syndrome left atrial pressure left bundle branch block lactate dehydrogenase liver function tests luteinizing hormone lithium dilution cardiac output [monitor] laryngeal mask airway low-molecular-weight heparin lumbar puncture lower respiratory tract infection lysergic acid diethylamide left ventricle/ventricular left ventricular assist device left ventricular end-diastolic pressure left ventricular failure left ventricular stroke work index microangiopathic haemolytic anaemia monoamine oxidase inhibitor mean arterial pressure molecular adsorbent recirculating system motorbike accident middle cerebral artery

SYMBOLS AND ABBREVIATIONS

MCH MCV MDMA MDR MEN MERiT MET MH MI MIBG MODS MOF MPAP MR MRDT MRI MRSA MSSA MSU MuSK MUST Na+ NaHCO3 NBM NG/NGT NIBP NIHSS NIV NJ nNRTI NPAs NPIS NRTI NSAIDs NSTEMI O2 OCP OD ODC OGT

mean cell haematocrit mean cell volume methylenedioxymethamphetamine (ecstasy) multiple drug resistance multiple endocrine neoplasia medical emergency response team medical emergency team malignant hyperpyrexia myocardial infarction metaiodobenzylguanidine [scan] multiple organ dysfunction syndrome multiple organ failure mean pulmonary artery pressure mitral regurgitation malaria rapid detection test magnetic resonance imaging meticillin-resistant Staphylococcus aureus meticillin-sensitive Staphylococcus aureus mid-stream urine muscle specific kinase malnutrition universal screening tool sodium sodium bicarbonate nil by mouth nasogastric (tube) non-invasive blood pressure National Institute of Health stroke score non-invasive ventilation naso-jejunal non-nucleotide reverse transcriptase inhibitors nasopharyngeal airways national poisons information service nucleotide reverse transcriptase inhibitors non-steroidal anti-inflammatory drugs non-ST elevation myocardial infarction oxygen oral contraceptive pill overdose oxygen dissociation curve oro-gastric tube

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SYMBOLS AND ABBREVIATIONS

OHSS OPAs P0.1 PINSP PA PaCO2 PACS PAFC PAN PaO2 PAOP/PAWP PAP PBO2 PC PCA PCA(S) PCI PCP PCR PCT PCWP PE PEA PEEP PEEPi PEFR PEG PET PFTs PI PICC PICH PIH PMH PMR PN PO POCS PPE

ovarian hyperstimulation syndrome oropharyngeal airways airway occlusion pressure at 0.1 seconds inspiratory pressure (mechanical ventilation) pulmonary artery partial pressure of arterial cardon dioxide partial anterior circulation syndrome pulmonary artery flotation catheter polyarteritis nodosa partial pressure of arterial oxygen pulmonary artery occlusion [or wedge] pressure pulmonary artery pressure brain tissue oxygen tension platelet concentrate posterior cerebral artery patient controlled analgesia (system) percutaneous coronary intervention (e.g. angioplasty) Pneumocystis jiroveci (carinii) pneumonia polymerase chain reaction or [urinary] protein:creatinine ratio procalcitonin pulmonary capillary wedge pressure pulmonary embolus or phenytoin equivalents pulseless electrical activity positive end-expiratory pressure intrinsic positive end-expiratory pressure peak expiratory flow rate percutaneous endoscopic gastrostomy pre-eclamptic toxaemia pulmonary function tests protease inhibitor peripherally inserted central catheter primary intracerebral haemorrhage pregnancy-induced hypertension past medical history polymyalgia rheumatica parenteral nutrition per os (orally) posterior circulation syndrome personal protective equipment

SYMBOLS AND ABBREVIATIONS

PPH PR PRN PSV PT PTH PUO PV PVL PVR PVRI QTc RA RAP RASS RBBB RBC REJ RIJ ROSC RPP RR RRT RS RSI RSV RSVP RTA R-tPA RUQ RV RVEDP SAFE SAH SaO2 SARS (-CoV) SBAR SBP SBT

postpartum haemorrhage per rectum (rectally) pro re nata (as required) pressure support ventilation prothrombin time parathyroid hormone pyrexia of unknown origin per vagina Panton–Valentine leucocidin pulmonary vascular resistance pulmonary vascular resistance index corrected QT interval rheumatoid arthritis or right atrium right atrial pressure Richmond agitation sedation assessment right bundle branch block red blood cell right external jugular right internal jugular return of spontaneous circulation rate pressure product respiratory rate renal replacement therapy respiratory system rapid sequence intubation respiratory syncytial virus Reason Story Vital signs Plan road traffic accident or renal tubular acidosis recombinant tissue plasminogen activator right upper quadrant right ventricle/ventricular right ventricular end-diastolic pressure Shout for help, Approach with caution, Free from danger, Evaluate ABC subarachnoid haemorrhage arterial oxygen saturation severe acute respiratory syndrome (corona virus) Situation Background Assessment Recommendation spontaneous bacterial peritonitis Sengstaken–Blakemore tube

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SYMBOLS AND ABBREVIATIONS

SC ScvO2 SGC SIADH SICH SIRS SjO2 SJS SK SL SLE SNP SOB SpO2 SSRI STD STEMI SV SVC SVI SvO2 Sv¯O2 SVR SVRI SVT SVV T3 T4 TINSP TACO TACS TAD TB TBI TBV TCA TCD TCRE TEN TFTs

subcutaneous central venous O2 saturation Swan–Ganz catheter syndrome of inappropriate ADH [secretion] spontaneous intracerebral haemorrhage systemic inflammatory response syndrome Jugular venous bulb O2 saturation Stevens–Johnson syndrome streptokinase sublingual systemic lupus erythematosus sodium nitroprusside shortness of breath plethysmographic [skin] O2 saturation selective serotonin reuptake inhibitor sexually transmitted disease ST elevation myocardial infarction stroke volume superior vena cava stroke volume index venous O2 saturation mixed venous O2 saturation systemic vascular resistance systemic vascular resistance index supraventricular tachycardia stroke volume variation tri-iodothyronine thyroxine inspiratory time (mechanical ventilation) transfusion associated circulatory overload total anterior circulation syndrome transfusion associated dyspnoea tuberculosis traumatic brain injury total blood volume tricyclic antidepressants transcranial Doppler transcervical resection of the endometrium toxic epidermal necrolysis thyroid function tests

SYMBOLS AND ABBREVIATIONS

TGI TIA TICA TICTAC TIPSS TLC TLS TOD TOE Toxbase t-PA TPN TR TRALI TSH T-spine TT TTE TTP TUR(P)(T) TV U&Es UOP URTI US UTI VAP VC VE VE VF VHF VMA VO2 V-P shunt VQ mismatch VISA VRE VRSA VRSS

tracheal gas insufflation transient ischaemic attack terminal internal carotid artery a tablet identification database transjugular intrahepatic porto-systemic shunting total lung capacity tumour lysis syndrome transoesophageal Doppler transoesophageal echocardiogram a toxicology database tissue plasminogen activator total parenteral nutrition (see PN) tricuspid regurgitation transfusion related acute lung injury thyroid-stimulating hormone thoracic spine thrombin time transthoracic echocardiogram thrombotic thrombocytopaenic purpura transurethral resection (of prostate or tumour) tidal volume urea and electrolytes urine output upper respiratory tract infection ultrasound urinary tract infection ventilator-associated pneumonia vital capacity minute volume ventricular ectopic ventricular fibrillation viral haemorrhagic fever vanillylmandelic acid systemic oxygen consumption ventriculo-peritoneal shunt ventilation perfusion mismatch vancomycin insensitive Staphylococcus aureus vancomycin resistant enterococcus vancomycin resistant Staphylococcus aureus vasopressor resistant septic shock

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SYMBOLS AND ABBREVIATIONS

VSD VT vWF WBC WCC WFNS WHO WPW

ventricular septal defect ventricular tachycardia von Willebrand factor white blood cell white cell count World Federation of Neurological Surgeons World Health Organization Wolff–Parkinson–White [syndrome]

Chapter 1

Assessment and stabilization Assessment and immediate management of an emergency 2 Early further management 10

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CHAPTER 1

Assessment and stabilization

4/ 3/ 2 Assessment and immediate management of an emergency The assessment and immediate management of critically ill patients follows the established ABC approach (Approach/Airway, Breathing, Circulation). What follows is a brief summary of the ABC approach adapted for patients within a critical care environment, further details on each system are considered in individual chapters. Any deterioration during assessment and resuscitation should prompt a return to ‘A’. Some interventions may need to be performed whilst continuing assessment and emergency treatment, particularly when emergencies are acute and life threatening (e.g. BLS/ALS, see b p.98; needle thoracocentesis of a tension pneumothorax, b p.80).

Approach • In all cases it is essential to ensure that those treating the patient are safe to carry out their work. • C-spine immobilization is often required where trauma is involved. • Give 100% oxygen in acute emergencies, in less acute scenarios titrate the oxygen required to keep SpO2 94–98%. • Connect any monitoring available—aim to have SpO2, continuous ECG, and non-invasive BP monitoring as a minimum: • Review any information from the monitoring devices (e.g. SpO2, ventilatory parameters, heart rate and rhythm, BP) alongside physical findings when examining the patient • Be alert for equipment malfunction (e.g. airway occlusion, ventilator failure, or infusion pump failure); and/or alarms from the monitoring systems which may indicate the cause or extent of problem • Obtain a history and detailed information about the patient: • From the patient where possible—the minimum history should include the ‘AMPLE’ template advocated in trauma resuscitation • From attending staff or from any associated documentation • Review notes, observation charts, imaging and blood results—fluid balance, blood gases, electrolytes • Physiological scoring systems (e.g. early warning scores, EWS, or ‘track and trigger’ systems) may be used to ‘flag’ up patients at high risk of deterioration (see b p.9) • Assess the existing level of support required by the patient (e.g. requirement for inotropes or haemofiltration)

The ‘AMPLE’ history • • • • •

A Allergies M Medication P Past medical history L Last meal E Event (and environment)

ASSESSMENT AND IMMEDIATE MANAGEMENT OF AN EMERGENCY

Airway The commonest cause of airway emergencies is airway obstruction. It may be partial or complete. In the unintubated patient • Assess the ability of the patient to breathe, or in conscious patients the ability to speak, listening for: • Silence (caused by apnoea or complete obstruction), or abnormally quiet breath sounds • Stridor, wheeze, or gurgling • A hoarse voice (associated with laryngeal oedema) • In unconscious or uncooperative patients feel for breath with your hand or cheek, check for misting on an oxygen mask. • Look for evidence of airway obstruction: • Bleeding, vomit, secretions, tissue swelling, or foreign bodies • Obstruction of the pharynx by the tongue • Look for neck swelling or bruising, surgical/subcutaneous emphysema, or crepitus • Look/listen for chest and other signs of airway obstruction, including: • Paradoxical chest and abdominal movements, tracheal tug • Reduced air entry in chest • Use of accessory muscles of respiration • Hypoxia is a late sign and indicates extreme emergency • Exclude obstruction of pharynx by the tongue: • Chin lift: useful for infants, edentulous or unconscious patients • Jaw thrust: generally more effective than chin lift, and can be done one-handed (skilled) or two-handed (unskilled) • Consider airway adjuncts: • Oropharyngeal (‘Guedel’) airways are normally only tolerated by unconscious patients • Nasopharyngeal airways are tolerated by conscious patients but may cause nasal bleeding on insertion worsening airway problems • Laryngeal mask airways (LMAs) require basic training to use, are only tolerated by unconscious patients, and offer limited protection from aspiration • Orotracheal intubation is the gold-standard for protecting and maintaining the airway but is only tolerated by anaesthetized or unconscious patients and requires a skilled operator to insert (the nasotracheal route is rarely required outside operating theatres) • Using a self-inflating bag and mask to assist ventilation, if possible, may allow time to look for or treat causes of obstruction. • Consider endotracheal intubation or an emergency needle cricothyroidotomy/tracheostomy (see b pp.522 and 528): • Specialist anaesthetic and/or ENT airway skills will also be required at this point • In patients who are unconscious, but maintaining an airway, endotracheal intubation should be considered, or the recovery position should be adopted (or alternatively ‘head-down, left lateral’ if they are lying on a trolley/bed).

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CHAPTER 1

Assessment and stabilization

In the intubated, mechanically ventilated patient Work methodically from the ventilator to the patient: • Check the ventilator is working (with adequate pressures, tidal volumes, and minute volumes) and that O2 is connected, check that ventilator tubing is still connected and not obstructed. • High airway pressure ventilator alarms may indicate obstruction. • Low pressure, or low expired volume alarms may indicate a leak. • Listen for any air leaks from ventilator tubing or endotracheal cuff. • Check the endotracheal tube (ETT): • ETT position is normally 20–22cm at lips (compare with any previously noted length), i insertion depth may indicate endobronchial placement. If immediately available, review CXR films to confirm correct placement of tube • Check tube patency (by passing a suction catheter through the endotracheal tube to exclude obstruction) • Laryngoscopy may be required to confirm correct placement • Check end-tidal CO2 to confirm ETT position (provided there is also adequate cardiac output) • Disconnect from ventilator and try ventilating with a self-inflating bag (successful ventilation indicates obstruction at the level of ventilator tubing): • If unsuccessful then there is an obstruction within or beyond the ETT, consider re-intubating with a fresh ETT and/or passing a fibreoptic scope; also consider causes for failure to expand the lungs (e.g. tension pneumothorax or bronchospasm) • Unilateral chest movement may be associated with pneumothorax or endobronchial intubation.

Breathing Common causes of breathing difficulties include pleural diseases (pneumothorax, haemothorax, or pleural effusion), airway diseases (asthma, secretions, acute exacerbation of COPD), parenchymal disease (collapse, consolidation, ARDS) and cardiogenic disease (cardiogenic pulmonary oedema). Evidence of inadequate breathing should be looked for and corrected, including: • Hypoxia—reduced PaO2 or SaO2. • Dyspnoea and/or tachypnoea (bradypnoea or Cheyne–Stokes breathing are late/severe signs). • Obvious problem, e.g. regurgitation with aspiration, massive bleeding. • Absent or abnormal chest movement: • Unilateral movements may indicate pneumothorax, pleural effusion, collapse • Paradoxical chest-abdominal movement may indicate airway obstruction or flail chest • Use of accessory muscles of respiration • Raised JVP may be visible. • Apex beat or tracheal shift may be seen towards areas of collapse or away from pneumothoraces or pleural effusions.

ASSESSMENT AND IMMEDIATE MANAGEMENT OF AN EMERGENCY

• Percussion may reveal effusions or pneumothoraces. • Abnormal breath sounds may be heard on auscultation: • Silent chest or wheeze may be due to acute severe asthma/ bronchospasm (pulmonary oedema may also cause wheeze) • Rattling noises suggests secretions • Absent unilateral sounds may be due to pleural effusion • Bronchial breathing suggests underlying consolidation • Patients should be asked to cough to assess their ability to clear secretions which may be limited by neuromuscular problems or pain. • Secretions themselves should be examined where possible, and patients encouraged to ‘cough up’ samples • Check any intercostal drains—check if drains are still swinging or bubbling, and check the volume of blood or serous discharge • Emergency management should be aimed at: • Excluding/treating life-threatening conditions (e.g. acute severe asthma, tension pneumothorax, pulmonary oedema, massive haemothorax) 1 • Keeping SaO2 94–98%, PaO2 >9 kPa, and PaCO2 within the normal limits for the patient with respiratory rate 2 seconds) • Alternatively a bounding pulse may occur with hypotension in individuals capable of compensating • Bradycardia is a pre-terminal sign, or a sign of vagal stimulation, (e.g. from intraperitoneal blood) • JVP may be raised • Other signs: • Tachypnoea, altered mental state • durine output (10 seconds) awakening, with eye contact, to voice Light sedation (briefly, 7 days old will remain patent and ventilation may be assisted via the stoma • If tracheostomy >7 days old attempt to resite the tracheostomy as soon as possible • Use fibreoptic bronchoscope ± airway exchange catheter to re-insert tracheostomy under direct vision • If this is not possible consider endotracheal intubation

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CHAPTER 2

Airway

In the event of airway bleeding: • Call for skilled help—senior anaesthetist and ENT. • Assess degree of bleeding and extent of lung soiling. • Fibreoptic laryngoscopy or bronchoscopy to assess the source of haemorrhage. • If minor bleeding from tracheostomy site: • Apply direct pressure ± suture to obvious bleeding point. If still bleeding consider soaking a haemostatic dressing (e.g. Kaltostat®) in 1 in 80,000 adrenaline and pack bleeding site • If major stoma bleeding: • Suction upper airway and tracheostomy to remove clots • Orally intubate, use uncut tube and ensure cuff is inflated below tracheostomy stoma • Achieve haemostasis of stoma using digital pressure, packing, or sutures • Arrange theatre for definitive haemostasis • Urgent endoscopy may be required to remove clots from airway and lungs • If major bleeding occurs late it may be due to erosion of right brachiocephalic artery (usually preceded by insignificant sentinel bleed): • Bleeding can by massive and life threatening • 100% oxygen, call for senior help • Suction airway • Inflate tracheostomy cuff with up to 50 ml air to provide local tamponade • Apply digital pressure to root of neck in sternal notch • Commence IV fluid resuscitation, cross-match blood • Arrange an emergency theatre team, may also require vascular and cardiothoracic surgeons If ever in doubt, secure airway using endotracheal intubation. Once Airway and Breathing are stabilized, continue ABC approach: • Check to ensure adequate ventilation, if poor consider the possibility of pneumothorax. • Urgent endoscopy may be required to remove clots from airway and lungs. • Fluid/colloid/blood to restore circulatory volume. • Correct any coagulopathy if there is airway bleeding.

Further management If condition is stable and any severe airway obstruction has been relieved: • Continue ventilation in an ICU setting. • If obstruction only mild or after the airway is re-established using ETT: • Re-explore tracheostomy wound and re-insert tube, this can be difficult, particularly via recent (180/110 mmHg); this may be managed by: • Treating pain (e.g. using IV diamorphine/morphine/fentanyl) • Increasing sedation (in ventilated patients) • Commencing an IV GTN infusion • Titrating 1–5 mg metoprolol IV

Absolute contraindications to thrombolysis • • • • • • • • •

Aortic dissection suspected. Active GI bleeding within the past 2 weeks. Major surgery or trauma in previous 6 weeks. Puncture of a non-compressible vessel or organ biopsy within the past 2 weeks. Previous haemorrhagic stroke. Ischaemic stroke within the previous 3 months. History of intracranial lesion. Anticoagulation with an INR >2; or known bleeding disorder. Recent central neuraxial blockade (e.g. within the past 12 hours).

Further management • Admit to a CCU, HDU, or ICU dependent on airway/breathing status. • Check serial ECGs and cardiac enzymes (including troponin at 12 hours); ECGs may identify an evolving STEMI, elevated troponin indicates an NSTEMI or STEMI. • Observe for new ST-segment and T-wave changes or left bundle branch block (initial ECG may be normal in 10–20% cases of MI) • Observe for the formation of pathological Q waves (hours to days) • Where thrombolysis has been performed repeat the 12-lead ECG after thrombolysis to ensure > 50% resolution of ST changes; if it does not, rescue angioplasty should be considered • Monitor for complications of MI (murmurs, arrhythmias, heart failure, pericardial effusion) and its treatment (GI haemorrhage). • Further chest pains, dynamic ECG changes, new heart failure, or valvular dysfunction should prompt cardiology consultation; further antiplatelet and/or anticoagulant therapy, or emergency coronary intervention may be indicated: • GP2b3a inhibitor infusion (e.g. eptifibatide, tirofiban, abciximab) • Calcium channel antagonist for continuing angina • Coronary reperfusion therapies (e.g. angioplasty and/or coronary stenting, or surgical coronary artery bypass grafting) • Continue/commence ACS medical therapies: • Aspirin and clopidogrel/prasugrel, β-blockers, ACE inhibitor, statins • LMWH/fondaparinux (this may be discontinued at day 8 after successful revascularization) • Once stabilized on other therapies wean GTN; if it is required for >24 hours allow ‘nitrate free’ periods to reduce nitrate tolerance

ACUTE CORONARY SYNDROMES

• Be vigilant to the further complications of bradycardia and heart block, tachyarrhythmias, LVF, pericarditis, DVT and PE, cardiac tamponade, MR, VSD, Dressler’s syndrome, and LV aneurysm. • If the patient requires CABG, clopidogrel/heparins/GP2b3a inhibitors should be stopped prior to surgery—be guided by cardiologist/cardiac surgeon/cardiac anaesthetist. • Consider TTE/TOE post infarction to assess LV function/valve status. • Avoid hyperglycaemia, maintain blood glucose 0.2 seconds (does not require treatment). • Second degree: • Mobitz type I (Wenkebach): PR interval gradually lengthens with each beat until there is an absent QRS following a P wave; the cycle then repeats • Mobitz type II: PR interval remains the same, intermittently there is failure of AV conduction and no QRS follows a P wave • Complete heart block: there is complete dissociation between P waves and QRS complexes; where the ventricle establishes its own ‘escape’ rhythm the QRS complexes are wide (>0.12 seconds) and the heart rate is typically 20–40 beats/minute (occasionally a nodal escape rhythm is established and QRS complexes may be narrow with heart rate around 50–60 beats/minute).

Differential diagnoses • Equipment failure, electrical interference (e.g. shavers, diathermy). • Any cause of shock, heart failure, or a terminal bradycardia (e.g. bronchospasm, head injury, tension pneumothorax). • PEA if cardiac arrest occurs.

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Immediate management (see also Fig. 4.3) Give 100% O2 initially, then titrate to SpO2 94–98%. Secure the airway and ensure breathing/ventilation is adequate. Confirm bradycardia by palpating pulse. Obtain IV access and attach cardiac monitoring or pacing defibrillator. • Record 12-lead ECG with a rhythm strip. • Correct any immediately reversible cause (e.g. warming, electrolytes). • Temporary pacing wires are often left in situ following cardiac surgery; pacing via these is first-line therapy. • • • •

If there are no adverse features and risk of asystole is low: • Observe, monitor, reverse obvious causes, seek cardiologist advice. If there are adverse features or risk of asystole is high: • Give atropine 500 mcg IV, repeat as necessary to a maximum of 3 mg: • Glycopyrronium bromide 200–600 mcg IV may be used as an alternative. • If this is ineffective commence other chemical treatments whilst arranging transvenous pacing: • Adrenaline infusion 2–10 mcg/minute IV, titrate to response, or • Isoprenaline 1–10 mcg/minute IV, or • Dopamine dose 5–20 mcg/kg/minute IV, or • Aminophylline 0.5 mg/kg/hour IV, or • Transcutaneous/external pacing • Transvenous pacing should be performed by a cardiologist as soon as possible for those patients dependent on chemical/external pacing. Transcutaneous/external pacing: • Use a defibrillator with transcutaneous pacing function. • Attach pads to dry skin (sternum/apex, or anterior/posterior). • Choose fixed mode (consider demand, if available, once stable). • Set the rate for 60–90/minute. • Increase the output (in mA) until capture occurs: pacing spikes are seen and QRS complexes are triggered by them. • Ensure there is mechanical capture (a pulse present with QRS complexes), otherwise treat for PEA. • Muscle twitching is normal; analgesia may be required if there is pain. Specific treatments: • Glucagon 1–5 mg IV (slow), or 1–7.5 mg/hour, may be used if bradyarrhythmia is caused by β-blockers or calcium channel blockers. • Calcium chloride 10 ml 10% IV for calcium channel blocker overdose. • Administer sodium bicarbonate 50 ml 8.4% solution IV for tricyclic antidepressant overdose. • Give digoxin-specific antibody fragments if digoxin toxicity is present. • If LA toxicity thought likely give Intralipid® solution 1.5 ml/kg 20% solution, followed by infusion of 15 ml/kg/hour (see b p.493).

BRADYCARDIA

• • • •

Assess using the ABCDE approach Give oxygen if appropriate and obtain IV access Monitor ECG, BP, SpO2, record 12-lead ECG Identify and treat reversible causes (e.g. electrolyte abnormalities)

Yes

• • • •

Adverse features? Shock Syncope Myocardial ischaemia Heart failure

NO

Atropine 500 mcg IV Satisfactory response?

YES

NO

Interim measures: • Atropine 500 mcg IV repeat to maximum of 3 mg • Isoprenaline 5 mcg min–1 IV • Adrenaline 2–10 mcg min–1 IV • Alternative drugs * OR • Transcutaneous pacing

Seek expert help Arrange transvenous pacing

YES

Risk of asystole? • Recent asystole • Mobitz II AV block • Complete heart block with broad QRS • Ventricular pause >3s NO

Observe

*Alternatives include: • Aminophylline • Dopamine • Glucagon (if beta-blocker or calcium channel blocker overdose) • Glycopyrrolate can be used instead of atropine

Fig. 4.3 Adult bradycardia algorithm. UK Resuscitation Council guidelines 2010. Reproduced with the kind permission from the Resuscitation Council (UK).

Further management • Look for any other coexisting conditions, especially if signs and symptoms fail to respond to correction of heart rate. • Monitor for an evolving infarct with cardiac enzymes and serial ECGs.

Pitfalls/difficult situations • Complete heart block only rarely responds to drug therapy. • Treat bradyarrhythmias in cardiac arrests as PEA (b p.101), pacing should be considered for complete heart block but not asystole.

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• Agonal rhythm occurs in dying patients, characterized by slow, irregular, wide ventricular complexes, progressing through PEA to asystole.

Further reading Durham D, et al. Cardiac arrhythmias: diagnosis and management: the bradycardias. Crit Care Resusc 2002; 4: 54–60. Resuscitation Council (UK). Advanced life support, 6th edn. London: Resuscitation Council (UK), 2011.

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3 Tachycardia Tachycardia is defined as a heart rate >100 beats/minute. It is more likely to be pathological, and patients more likely to be compromised, at rates >150 beats/minute. Patients with pre-existing cardiac disease may be compromised to a greater extent, even at lower heart rates. Tachycardias can be sinus or tachyarrhythmias. The latter can be either broad complex or narrow complex (QRS), regular or irregular.

Types of tachyarrhythmias • Sinus tachycardia may occur (not strictly a cardiac arrhythmia). • Narrow complex ‘supraventricular’1 tachyarrhythmia (QRS 0.12 seconds): • Ventricular tachycardia (monomorphic) • Torsade de pointes (polymorphic VT) • Any cause of narrow complex tachycardia with aberrant conduction (e.g. SVT with bundle branch block, pre-excited AF) 1 The term supraventricular tachycardia (SVT) can represent any cause of narrow complex tachycardia, though in practice it most commonly refers to re-entrant tachycardia or ectopic atrial tachycardia.

Causes Sinus tachycardia may be a physiological response to: • Pain, anxiety, inadequate sedation, awareness (paralysed patients). • Sepsis and systemic inflammatory response, pyrexia. • Anaemia, hypovolaemia, haemorrhage, hypoxia, hypercapnia, PE. • Tension pneumothorax, tamponade. • Thyrotoxicosis. • Drug therapy (e.g. inotropes, pancuronium, salbutamol, aminophylline). • Drug intoxication (e.g. cocaine, ecstasy, amphetamines, TCAs, SSRIs). • Drug withdrawal (e.g. alcohol, opiate, benzodiazepines). Tachyarrhythmias (p cardiac: atrial or ventricular origin): • p cardiac disease: ischaemic heart disease, cardiomyopathy, valve disease, abnormal conduction (long QT syndrome: torsade de pointes). • Hypoxia, hypercapnia, acidaemia, hypovolaemia, shock, sepsis. • Electrolyte abnormalities, especially potassium and magnesium. • Thyrotoxicosis. • Extremes of temperature (hypothermia, hyperpyrexia). • Pulmonary artery catheterization or CVC line placement. • During or after cardiac surgery, revascularization, or defibrillation. • Drug therapy (e.g. inotropes, salbutamol, aminophylline).

TACHYCARDIA

• Drug toxicity (e.g. alcohol, cocaine, ecstasy, amphetamines, TCAs, SSRIs, local anaesthetic toxicity); drug interactions (e.g. tricyclics, macrolide antibiotics, antifungals, antipsychotics: torsade de pointes).

Presentation and assessment Patients may be asymptomatic, present in cardiac arrest, or have: • Anxiety and sweating. • Palpitations, chest pain, and/or ischaemia on ECG. • Tachypnoea, dyspnoea, hypoxia, cyanosis. • Hypotension (systolic BP 2 seconds) • Dizziness, syncope, dconsciousness • Oliguria • If heart failure is present: • Raised JVP (>4 cm from sternal angle) or CVP (>15 cmH2O) • Cannon ‘a’ waves may be seen in ventricular tachycardia (these are a sign of AV dissociation and are also seen in asymptomatic individuals in the absence of heart failure) • Gallop rhythm, S3 may be present • Enlarged and tender liver, ascites and oedema of dependent areas (e.g. legs or sacrum) may be present • Haemodynamic measurements may reveal dcardiac output and isystemic vascular resistance. • If pulmonary oedema is present: • Patient may prefer sitting, or leaning forward (orthopnoea) • Cough and/or frothy pink sputum • Bilateral crackles and/or wheeze • There may be difficulty ventilating patients on IPPV.

Investigations • 12-lead ECG with rhythm strip (determine QRS width and regularity; compare with old ECGs). • ABGs (hypoxia, hypercapnia, metabolic acidosis). • FBC (anaemia). • U&Es, (hyperkalaemia, hypokalaemia). • LFTs, TFTs, serum magnesium, calcium, phosphate, glucose. • D-dimer (may rule out PE in low probability cases). • Cardiac enzymes/troponin, after 12 hours (can be raised following tachyarrhythmias, but persistent ECG/echocardiography changes may suggest MI as cause). • CXR (pulmonary oedema, pneumothorax, pneumonia, cardiac size). • Consider echocardiography once stable and heart rate controlled (structural heart disease, signs of infarction, and functional assessment).

Differential diagnoses • Interference from equipment or patient (e.g. CVVH, shivering, tremor). • Any cause of sudden hypotension (e.g. haemorrhage or anaphylaxis). • Sinus tachycardia as a response to trauma, or sepsis, is often mistaken for SVT. SVT is more likely if: onset is sudden, rate is very high, rhythm is irregular, rhythm responds to treatment.

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Immediate management • Stop any triggers (e.g. drugs or procedures). • Check pulse; if a central pulse is absent treat as: • Narrow complex tachycardia: PEA (b p. 101) • Broad complex tachycardia: VF/pulseless VT (b p. 101) • Give 100% O2, secure the airway, ensure breathing/ventilation is adequate; endotracheal intubation may be required. • Obtain IV access and attach cardiac monitoring. • Record 12-lead ECG with a rhythm strip. • Correct reversible cause (e.g. electrolyte imbalance, hypoxia). • If it is a sinus tachycardia treat the cause, do not cardiovert.

If (non-sinus) tachyarrhythmia is present (See also Fig. 4.4.) If the patient has any of the following adverse features • Significant hypotension (systolic BP 48 hours old where rate control has been achieved, consider anticoagulation and/or TOE to identify any atrial thrombus before proceeding to elective cardioversion. • Look for any other coexisting conditions, especially if signs and symptoms fail to respond to correction of heart rate. • CVC position is a common cause of arrhythmias: confirm the position with a CXR, aiming for above the carina. • Consider obtaining an ECHO where structural heart disease or myocardial damage is suspected. • New AF is a common postoperative occurrence and may respond to fluid loading and magnesium bolus (as for torsade de pointes but over 20–30 minutes); magnesium may cause flushing and hypotension.

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Pitfalls/difficult situations • The emergency treatment of tachyarrhythmias with patient compromise is electricity: synchronized DC cardioversion x 3 attempts 200–360 J. • Any pulseless tachyarrhythmia besides VF/VT is treated as PEA. • Many critical care patients are already sedated/anaesthetized, proceeding directly to cardioversion may be more appropriate than drug therapy; where cardioversion has failed, consider repeating after normalization of electrolytes, or after treatment with amiodarone. • Sinus tachycardia is very common; at heart rates above 140 beats/ minute the ECG rhythm may be difficult to interpret (consider increasing recording speed to 50 mm/second to identify P-QRS-T).

Cardiac drugs Adenosine: • 6 mg IV as rapid bolus, followed by saline flush, if no response try two 12-mg boluses. • Side effects: flushing, chest tightness/bronchospasm, choking, nausea, bradycardia. • Contraindications: asthma, sick sinus syndrome, second- or third-degree heart block, AF or atrial flutter and pre-excitation syndromes, in heart transplant recipients. Amiodarone, loading dose 5 mg/kg IV (7300 mg) over 15–30 minutes, (in 100 ml 5% glucose, via CVC if possible), maintenance dose 15 mg/kg (7900 mg) over 24 hours. Digoxin, loading dose 0.75–1.0 mg IV over 1–2 hours (in 100 ml 5% glucose), maintenance dose of 0.0625–0.25 mg/day: • Adjust according to age, renal function, and drug interactions. • Contraindicated in AF or atrial flutter and pre-excitation syndromes. Esmolol loading dose 500 μg/kg IV over 1 minute, then 50–200 μg/kg/ minute. Magnesium IV replacement infusion 20 mmol (5 g) over 1–2 hours (in 100 ml 5% dextrose) via a central line: • Aim for a plasma concentration of 1.4–1.8 mmol/L. • In torsade de pointes consider giving 8 mmol (2g) in 100 ml 5% glucose IV over 2–5 minutes followed by an infusion of 2–4 mmol/ hour (0.5–1 g/hour). Potassium IV 40 mmol over 1–4 hours (in 10 ml 5% glucose) via a central line: • Aim for plasma concentration of 4.0–5.0 mmol/L. Verapamil IV 2.5–5 mg over 1 minute: • Avoid with re-entry tachycardia. • May cause profound hypotension if given to misdiagnosed VT or in hypotensive patients (or patients with LV dysfunction). • May cause profound bradycardia in combination with β-blockade.

• • • •

Assess using the ABCDE approach Give oxygen if appropriate and obtain IV access Monitor ECG, BP, SpO , record 12-lead ECG 2 Identify and treat reversible causes (e.g. electrolyte abnormal

Yes / Unstable

Synchronised DC Shock Up to 3 attempts

• •

Amiodarone 300 mg IV over 10–20 min and repeat shock; followed by: Amiodarone 900 mg over 24 h

Shock Syncope Myocardial ischaemia Heart failure

No / Stable Broad

Irregular

Adverse features?

• • • •

Broad QRS Is rhythm regular?

Is QRS narrow (< 0.12 s)?

Regular

Regular

• • Seek expert help

!

Narrow

•

Narrow QRS Is rhythm regular?

Use vagal manoeuvres Adenosine 6 mg rapid IV bolus; if unsuccessful give 12 mg; if unsuccessful give further 12 mg. Monitor ECG continuously

Sinus rhythm restored? Possibilities include: AF with bundle branch block treat as for narrow complex

•

Pre-excited AF consider amiodarone

•

Polymorphic VT (e.g. torsade de pointes – give magnesium 2 g over 10 min)

If previously confirmed SVT with bundle branch block: • Give adenosine as for regular narrow complex tachycardia

Yes

Irregular Narrow Complex Tachycardia Probable atrial fibrillation Control rate with: • β-Blocker or diltiazem • Consider digoxin or amiodarone if evidence of heart failure

No Seek expert help

Probable re-entry paroxysmal SVT: • Record 12-lead ECG in sinus rhythm • If recurs, give adenosine again & consider choice of anti-arrhythmic prophylaxis

Possible atrial flutter • Control rate (e.g. β-Blocker)

Fig. 4.4 Adult tachycardia (with pulse) algorithm. UK Resuscitation Council guidelines 2010. Reproduced with the kind permission from the Resuscitation Council (UK).

! TACHYCARDIA

•

If ventricular tachycardia (or uncertain rhythm): • Amiodarone 300 mg IV over 20–60 min; then 900 mg over 24 h

Irregular

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Further reading Blomström-Lundqvist C, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias – executive summary. Eur Heart J 2003; 24: 1857–97. Camm JA, et al. Guidelines for the management of atrial fibrillation. Eur Heart J 2010; 31: 2369–429. Resuscitation Council (UK). Advanced life support, 6th edn. London: Resuscitation Council (UK), 2011. Zipes DP, et al. ACC/AHA/ESC 2006 Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden death – executive summary. Eur Heart J 2006; 27: 2099–140.

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4 Cardiac tamponade Tamponade occurs when blood/fluid accumulates in the pericardium and impairs cardiac output. The rapid accumulation of 100–200 ml may cause acute tamponade; up to 1000 ml may build up in chronic tamponade.

Causes Acute • Blunt or penetrating thoracic trauma. • Recent cardiac surgery/catheterization/pacing, or CVC insertion. • Dissecting aortic aneurysm, or cardiac rupture after an acute MI. • Coagulopathy (e.g. thrombocytopaenia/uraemia/anticoagulation). Chronic • Metastatic disease; or following radiotherapy. • Pericarditis (idiopathic, uraemia, or connective tissue disorders/SLE). • Infection (e.g. bacterial, viral, fungal, TB, HIV). • Hypothyroidism.

Presentation and assessment May present as cardiac arrest. Anxiety, restlessness, and/or palpitations. Respiratory distress: tachypnoea, dyspnoea and cyanosis. Dizziness, syncope, dconsciousness. Chest pain which is relieved by sitting upright and leaning forwards. Tachycardia, hypotension, peripheral oedema or poor perfusion. Raised JVP/CVP; especially with a prominent ‘x’ descent and loss of ‘y’ descent (Kussmaul’s sign). • dpulse pressure, pulsus paradoxus, loss of radial pulse on inspiration. • Muffled heart sounds or a pericardial rub. • Elevated and equalized ventricular filling pressures (CVP/PAOP). • • • • • • •

Investigations ABGs (metabolic acidosis). FBC (iWCC in pericarditis, thrombocytopaenia). Coagulation screen (deranged in anticoagulation). U&Es (uraemia, AKI); LFTs (deranged if hepatic congestion present). ECG (low voltage with electrical alternans or T-wave changes). Echocardiography, TTE or TOE (visible pericardial fluid, small ventricles with impaired filling, diastolic collapse of right ventricle). • CXR (widened mediastinum or globular heart); CT/MRI chest. • PAFC/TOD (low cardiac output, high SVR, and high PCWP). • Cytology and culture of pericardial fluid. • • • • • •

Differential diagnoses • Sudden cardiovascular collapse (e.g. tension pneumothorax, pulmonary embolus, anaphylaxis, air trapping in acute severe asthma). • dcardiac output (e.g. cardiogenic shock, myocardial failure, myocardial infarction, constrictive/restrictive pericarditis). • Volume overload; SVC obstruction.

CARDIAC TAMPONADE

Immediate management • Give 100% O2 initially, then titrate to SpO2 of 94–98%. • Secure the airway and ensure breathing is adequate; endotracheal intubation and ventilation may be required. • Ensure adequate IV access and administer an IV fluid challenge. • Commence inotropic support if patient remains shocked. • Under no circumstances remove any penetrating foreign body. • Monitor the patient’s ECG. Imminent/actual cardiac arrest • Commence basic/advanced life support. • Perform emergency pericardiocentesis (b p. 546). Post cardiac surgery (See b p. 394.) • Clear any obstruction to chest drains. • Call for surgical help, alert theatres, obtain wire cutters. • Administer anaesthesia prior to chest opening using the most cardiostable induction agents/analgesics (be prepared to open chest immediately post induction). • Intubate and ventilate (if patient is not already). • If cardiac arrest occurs, reopen chest immediately. • Ensure blood and clotting factors are available/requested. Other situations • Arrange urgent ECHO to confirm tamponade. • Proceed to immediate ECHO-guided pericardiocentesis if: • ECHO shows >1.5 cm fluid plus diastolic collapse • Seek cardiology advice if: • ECHO shows 1.5 cm fluid but no collapse • ECHO shows effusion with dilated LV

Further management • • • • •

Avoid bradycardia, maintain filling pressures and sympathetic tone Correct metabolic acidosis. IPPV may worsen hypotension and tamponade. Antibiotic prophylaxis will be needed if the chest has been opened. Follow-up cytology and culture of pericardial fluid.

Pitfalls/difficult situations • An indwelling pericardiocentesis catheter, or creation of a pericardial window or pericardectomy may be required in some patients. • Pulmonary oedema may occur after drainage of tamponade. • Low pressure tamponade can occur; in these cases JVP is not elevated, RAP is normal, and the patient may respond to IV fluids. • Ensure wire cutters are available for cardiac surgery patients. • Echocardiography is the investigation of choice to diagnose tamponade.

Further reading Bodson L, et al. Cardiac tamponade. Curr Opin Crit Care 2011; 17(5): 416–24. Spodick DH Current concepts: Acute cardiac tamponade. N Engl J Med 2003; 349: 684–90.

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3 Hypertensive crises Moderate hypertension is a common finding in critical care patients and rarely needs aggressive management. Hypertensive crises (or emergencies) with end-organ dysfunction require urgent IV treatment to prevent associated morbidity/mortality.

Causes Hypertension may be as a result of: • p hypertension (no identifiable underlying cause). • s hypertension: • Drugs (e.g. cocaine, sympathomimetics) • Renal/renovascular disease • Endocrine (e.g. phaeochromocytoma or Cushing’s syndrome) • Coarctation • Pregnancy, pre-eclampsia/eclampsia • Reactive hypertension (pain, anxiety, hypercapnia). Severely elevated blood pressure equates to: systolic >180 mmHg, or diastolic >110 mmHg (sometimes referred to as hypertensive urgencies). Hypertensive crisis occurs when hypertension causes acute end-organ dysfunction (see b Presentation and assessment).

Presentation and assessment End-organ dysfunction includes: • Neurological dysfunction (headache, blurred vision, papilloedema, fundal haemorrhages, encephalopathy, limb weakness). • ACS, acute myocardial infarction. • Aortic dissection. • Pulmonary oedema. • Acute kidney injury. • Microangiopathic haemolytic anaemia. • Pregnant patients: pre-eclampsia/eclampsia, or HELLP syndrome (see b pp. 432 and 436). Critically ill patients with a BP of >220 mmHg systolic or >130 mmHg diastolic should be reviewed to exclude end-organ damage.

Investigations • • • • • • • • •

ABGs (metabolic acidosis). FBC, coagulation screen, fibrinogen (MAHA, DIC). U&Es (raised urea/creatinine/hyperkalaemia). LFTs, TFTs (hyperthyroidism), blood glucose (hyperglycaemia). Urine dipstick (haematuria and/or proteinuria). Urine/blood βHCG (to exclude pregnancy/eclampsia). ECG (cardiac ischaemia, LVH), CXR (pulmonary oedema). CT head (to rule out other causes of encephalopathy). Renal US/Doppler, renal angiography (CT or MRI).

Differential diagnoses • Coincidental hypertension (e.g. alongside MI, or encephalitis).

HYPERTENSIVE CRISES

Immediate management • Ensure airway, breathing, and circulation are stabilized. • Treat any underlying cause, in particular: • Ensure adequate analgesia and/or adequate sedation/anaesthesia, particularly where neuromuscular blockade is being used • Follow the protocols for suspected phaeochromocytoma (b p.244), thyroid storm (b p.238), or pre-eclampsia (b p.432) • If hypertensive crisis is present (with end-organ damage) reduce MAP by 10–20% MAP (greater reductions may cause complications): • Insert an arterial line for continuous BP measurement • Use short-acting IV drug infusions to achieve initial BP control to allow rapid discontinuation if necessary Drug choices: • Glyceryl trinitrate (GTN) 0.5–20 mg/hour IV, titrated to effect (venodilator, half-life 3 minutes; side effects: tachycardia, headache, and tolerance). • Sodium nitroprusside (SNP) 0.25–10 mcg/kg/minute IV titrated to effect (vasodilator, half-life 2 minutes, side effects include tachycardia and cyanide toxicity, giving sets need to be protected from sunlight). • Esmolol hydrochloride 500 mcg/kg/minute IV for 1 minute, followed by 50–300 mcg/kg/minute IV titrated to effect (β-blocker, half-life 8 minutes, side effects include bradycardia and bronchospasm). • Labetalol hydrochloride 20 mg IV over 2 minutes, followed by an infusion at 2 mg/minute until a satisfactory response is obtained; maximum dose 300 mg (combined alpha1 and non-selective β-blocker, half-life 4 hours, side effects include bradycardia and bronchospasm, caution in impaired hepatic function). • Hydralazine 5–10 mg by slow IV bolus, repeated after 15 minutes, followed by an infusion at 5–15 mg/hour (arteriolar vasodilator, half-life 2–4 hours, less tritratable). Hypertension should not be aggressively treated when it occurs as a response to raised intracranial pressure i.e. following head injury.

Further management • Once BP control is achieved consider longer-term antihypertensive therapy, e.g. ACE inhibitors, β-blockers, diuretics.

Pitfalls/difficult situations • Sublingual nifedipine should be avoided for the treatment of severe hypertension as it may cause precipitous drops in BP. • Hypertension as a consequence of acute neurological events is difficult to manage; treatment depends upon the underlying pathology. • Combinations of drugs may be more effective (e.g. β-blocker and vasodilator), and alternative drugs infusions include phentolamine or fenoldapam; diuretics are not recommended.

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• Mild hypoperfusion may cause ischaemia in patients with cerebrovascular or carotid disease; treatment should be aimed at reducing MAP by a maximum of 20%.

Further reading Cherney D, et al. Management of patients with hypertensive urgencies and emergencies. J Gen Intern Med 2002; 17: 937–45. Marik P, et al. Hypertensive crises: challenges and management. Chest 2007; 131; 1949–62. Perez MI, et al. Pharmacological interventions for hypertensive emergencies. Cochrane Database Syst Rev 2008; 1: CD003653. DOI: 10.1002/14651858.CD003653.pub3. Santhi R, et al. Hypertension in the critically ill patient. Critical Care Resusc 2003; 5(1): 24–42.

Chapter 5

Neurology Decreased consciousness 152 Seizures and status epilepticus 160 Stroke/thromboembolic stroke 166 Intracerebral haemorrhage 172 Subarachnoid haemorrhage 174 Traumatic brain injury 178 Raised intracranial pressure 186 Meningitis and encephalitis 188 Agitation/confusion/aggression 192 Alcohol withdrawal 194 Neuromuscular weakness and paralysis 196 Guillain–Barré syndrome 198 Myasthenia gravis 200

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3 Decreased consciousness dconsciousness occurs in many diseases requiring admission to intensive care, and is often a cause for admission in its own right. Changes in neurological state may be related to intracranial pathology, or may occur in response to respiratory, circulatory, or metabolic disorders. The immediate management of dconsciousness should aim to protect the airway, ensure adequate respiration, prevent BP fluctuations, and maintain adequate oxygen delivery to the brain.

Causes Physiological derangement • Hypoxia. • Hypercapnia. • Hypotension. • Hypothermia/hyperthermia. • Hypoglycaemia/hyperglycaemia. • Other metabolic derangement (e.g. hyponatraemia/hypernatraemia, hypocalcaemia, hypermagnesaemia, hyper-osmolar states). • Endocrine disease (e.g. hypothyroidism/hyperthyroidism, Addison’s disease). • Hepatic failure, renal failure. Intracranial damage • Diffuse brain injury. • Extradural haemorrhage, subdural haemorrhage, intracerebral bleed. • Stroke/ischaemia. • Tumour/other intracerebral mass. • Cerebral oedema. Seizures • Status epilepticus, post-ictal states. Infections • Meningitis, encephalitis, intracranial abscess. • Systemic sepsis. Drugs and toxins • Alcohol, sedatives, illicit drugs.

Presentation and assessment Level of consciousness should be quantified using the Glasgow coma score (GCS) or AVPU systems (rather than poorly defined terms such as unconscious, semi-conscious, obtunded, comatose). GCS assesses eye, verbal and motor responses and has a maximum score of 15 (fully conscious) and a minimum score of 3 (deeply unconscious/comatose). A GCS 20 mmHg) where monitored.

Other signs and symptoms may include: • Airway: grunting, snoring, or complete obstruction may occur (airway obstruction may cause, or be caused by, loss of consciousness). • Respiratory: • Hypoventilation is a late sign unless associated with narcotic/drug overdose • Hyperventilation and/or Kussmaul’s breathing may indicate a metabolic acidosis (e.g. DKA) • Cheyne–Stokes is associated with brainstem events or raised ICP • Tachypnoea causing a respiratory alkalosis may sometimes occur • Neurogenic pulmonary oedema • Cardiovascular changes: • Tachycardia or hypotension may occur if there is associated trauma (especially spinal) • Bradycardia is often a late or pre-terminal sign • Hypertension may be associated with pain or agitation, or may be associated with severe neurological injury (more likely in patients who are deeply unconscious) • Cushing’s response of hypertension combined with bradycardia is a late sign indicative of severe intracranial hypertension • ECG changes: ischaemic changes can occur in association with subarachnoid or intracerebral bleeding; cardiac ischaemic events or arrhythmias (Stokes–Adams attacks) can cause dconsciousness; chronic AF is associated with thromboembolic events • Renal: incontinence, polyuria.

DECREASED CONSCIOUSNESS

Investigations • ABGs (for hypoxia, hypercapnia, acidaemia and anion gap). • FBC, coagulation screen (particularly in anticoagulated patients, or where acute liver failure is possible). • U&Es (especially to look for hyponatraemia or AKI, LFTs, CK). • Serum glucose, with urinalysis for ketones if indicated (may identify hypo-, hyperglycaemia, or HHS/HONK). • Plasma osmolality (may help identify ethanol, methanol, or ethylene glycol poisoning). • Crossmatch blood (if there is trauma or risk of bleeding). • Blood alcohol levels and/or urine toxicology (for illicit drugs). • Blood, urine, and sputum cultures where infection is a possible cause. • ECG (tachyarrhythmia or bradyarrhythmia). • CXR (malignancy or pneumonia may be present). • Lumbar puncture (usually after CT head, see b p.574). • CT head (and possible also neck, see b Criteria for the request for CT scan of the head and also p.182). • MRI head (investigation of choice for suspected brainstem lesions). • In patients with associated trauma also consider: C-spine X-rays, other trauma X-rays (e.g. pelvis or long bones), skull or facial X-rays. • CFAM/EEG may be indicated if status epilepticus is suspected.

Criteria for the request for CT scan of the head Immediate CT head scan for a head injury with any of the following: • GCS 30 minutes before a head injury. • Amnesia or loss of consciousness in the elderly or those with a coagulopathy (e.g. patients on warfarin). • Any injury with a suspicious mechanism (e.g. fall from height or ejection from a car). Other indications • Any prolonged, unexplained episode of dconsciousness or focal neurology. • History suggestive of subarachnoid haemorrhage, meningitis, encephalitis, or intracranial abscess. • Suspected stroke or other central neurological deficit. • Status epilepticus. • Raised ICP (if measured) resistant to treatment.

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Immediate management • Give 100% O2, supporting airway/breathing/circulation as required . • Use cervical spine precautions if trauma is suspected/possible. • Obtain a contemporaneous history if possible (e.g. from relatives or ambulance crew): • An ‘AMPLE’ history should be obtained as a minimum (b p.2) • Roughly assess neurological state (e.g. conscious and talking, or unconscious): • Simultaneously treat neurological complications which may interfere with ABC (e.g. seizures) • Complete basic ABC p survey before formally assessing neurological state. Airway • The airway may be compromised due to impaired conscious level: • Intubate the trachea as appropriate • If this is impossible (i.e. in a remote location) the patient may be placed in the recovery position (depending on the risk posed by other injuries) • If endotracheal intubation is required a rapid sequence intubation will be required to minimize the risk of aspiration. • The stress response to endotracheal intubation should be avoided if possible, by using induction agents/short-acting opiates. • Rapid sequence endotracheal intubation should be considered if: • GCS 8, or rapidly deteriorating • There is risk of aspiration of vomit or blood • There is a lack of gag reflex • There is facial or neck trauma putting the airway at risk • There is hypoxia (SaO2 13 kPa, and PaCO2 4.0–4.5 kPa should be maintained.

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• Pulmonary oedema may require the addition of PEEP (although caution may be required as high levels of PEEP may increase ICP). • Aspiration and chest infections are common in patients with dconsciousness and should be actively sought/treated. • Head-up positioning may decrease the risk of aspiration and improve cerebral venous drainage. Cardiovascular • Hypotension should be avoided; a MAP >90 mmHg should be sufficient initially: • MAP may be guided later by ICP (allowing calculation of CPP) or other measurements (see b p.186) • Fluid resuscitation (avoiding hypotonic fluids) is often sufficient, although inotropes may be needed. Sedation • Sedation will be required in most cases where patients are intubated and ventilated. • Sedatives with rapid offset (e.g. propofol) are useful initially as they can be discontinued and the level of consciousness rapidly reassessed. • Muscle relaxants may be required initially for endotracheal intubation, or for short periods during transfer or CT scanning; however, they run the risk of masking seizure activity: • Where neuromuscular blockade is used consider concurrent sedative infusions with anticonvulsive prophylaxis (e.g. propofol or midazolam), or CFAM/EEG monitoring. Metabolic • Hyper- or hypoglycaemia should be avoided. • Hyper- or hyponatraemia should be corrected (see b pp. 208 and 210). • Pyrexia should be avoided; the place of mild/moderate hypothermia for severe neurological injuries is unclear, but is practised by some hospitals (mild/moderate hypothermia following cardiac arrest is indicated, see guidelines, b p. 103).

Pitfalls/difficult situations Hypoglycaemia is a common treatable cause; every patient with dconsciousness should have a finger-prick blood sugar test. • Drug or alcohol use is frequently associated with other causes of diminished consciousness; a high suspicion of metabolic derangement or head injury/intracranial haemorrhage is essential in these patients. • Diminished consciousness is common in patients sedated in intensive care for prolonged periods, or where there has been renal or hepatic dysfunction leading to a prolonged washout period of sedative medications; a low threshold for suspecting metabolic derangement, intracranial haemorrhage/ischaemia is advisable. • Alcoholic and coagulopathic patients are at i risk of intracranial haemorrhage even after relatively minor trauma. • Transfer to CT or MRI is hazardous (particularly MRI where monitoring and ventilators need to be ‘magnet compatible’); scans should only be attempted once patients are stable.

DECREASED CONSCIOUSNESS

• In some cases general surgical interventions (e.g. for major internal haemorrhage) may take precedence over investigating or treating neurological problems.

Further reading Bateman DE. Neurological assessment of coma. J Neurol Neurosurg Psychiatry 2001; 71(SI): i13–i17. Holzer M. Targeted temperature management for comatose survivors of cardiac arrest. N Engl J Med 2010; 363: 1256–64. Mayer S, et al. Critical care management of increased intracranial pressure. J Intensive Care Med 2002; 17: 55–1767. Moppett IK. Traumatic brain injury: assessment, resuscitation and early management. Br J Anaesth 2007; 99(1): 18–31. NICE. Head injury. Triage, assessment, investigation and early management of head injury in infants, children and adults. London: NICE, 2007. Sanap MN, et al. Neurologic complications of critical illness: Part I. Altered states of consciousness and metabolic encephalopathies. Crit Care Resusc 2002; 4(2): 119–32. Scottish Intercollegiate Guidelines Network. Early management of patients with a head injury: a national clinical guideline. Edinburgh: Scottish Intercollegiate Guidelines Network, 2009. Sydenham E, et al. Hypothermia for traumatic head injury (review). Cochrane Database Syst Rev 2009; 2: CD001048. DOI: 10.1002/14651858.CD001048.pub4 Varon J, et al. Therapeutic hypothermia: past, present, and future. Chest 2008; 133: 1267–74.

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4 Seizures and status epilepticus Seizures require intensive care management if they are prolonged, are associated with underlying disease, or cause severe physiological disturbance. Prolonged seizure activity carries a significant mortality. Any seizure lasting >5 minutes should be treated as an emergency. A working definition of status epilepticus is: a seizure lasting >10 minutes, or repeated seizure activity without full consciousness between seizures, or failure to respond to 2 first-line treatments.

Causes • Hypoxia. • Brain injury (e.g. traumatic brain injury, intracranial tumour, haemorrhagic or ischaemic stroke, TTP). • Metabolic/electrolyte abnormalities (e.g. hypoglycaemia, hyperglycaemia, uraemia; sodium, calcium, or magnesium derangement). • Eclampsia (b p. 432). • Infection (e.g. meningitis, encephalitis, brain abscess). • Drug associated: drug withdrawal (especially alcohol), drug overdose, or illicit drug use (particularly cocaine). • In patients known to have epilepsy, seizures may be triggered by: • Head trauma, alcohol, intercurrent infection • Subtherapeutic blood levels of antiepileptic medications

Presentation and assessment Seizures are most commonly generalized convulsive, with: • Loss of consciousness. • Tonic–clonic muscle movements (these may become very subtle when prolonged seizure activity leads to exhaustion). • Subtle eye movements (sometimes the only sign). • Teeth clenching, tongue biting, and/or urinary incontinence. • Physiological response to seizure: • Sweating and/or hyperthermia • Tachypnoea (airway obstruction may occur; hypoxia is associated airway obstruction and with prolonged fits) • Tachycardia and hypertension • Organ failure: rhabdomyolysis, AKI, DIC Non-convulsive episodes are difficult to characterize, but may involve: • Impaired consciousness (defined as absence or complex seizures, and can range from lack of awareness to stupor). • Partial seizures: features may include focal twitching, facial tics, autonomic symptoms, and/or hallucinations (gustatory, acoustic, sensory, or visual), automatic behaviour (e.g. chewing, lip-smacking).

Investigations • • • • •

ABGs (hypoxia, metabolic acidosis, raised lactate). FBC, CRP (meningitis/encephalitis or intercurrent infection). Serum glucose. U&Es, LFTs, serum magnesium and calcium. CK (raised after prolonged fits).

SEIZURES AND STATUS EPILEPTICUS

Urine/blood βHCG (to exclude pregnancy/eclampsia). Blood and/or urine toxicology screen (for alcohol or illicit drugs). Serum anticonvulsant drug levels (in patients with known epilepsy). CXR (to exclude malignancy, infection, or aspiration). Head CT/MRI (if seizures are prolonged, or have no obvious precipitant; or if focal neurology, papilloedema, or head injury are present). • Lumbar puncture (if infection is possible/likely). • Blood, urine, and sputum cultures (if infection is likely). • EEG as advised by neurologists. • • • • •

Differential diagnoses • Any disease causing spasms (e.g. rigors, myoclonic jerks, dystonia). • Any disease causing syncope or agitation (see b pp.152 and 192). • Psychogenic seizures, also known as pseudoseizures (see b Pitfalls/ difficult situations).

Immediate management • Give 100% O2, monitor SpO2. • Airway may be compromised due to seizure activity: • Maintain airway until fit is terminated, adjuncts may be required (consider nasal airways where there is marked jaw clenching) • Consider placing the patient in recovery position • Ensure breathing/ventilation is adequate (in some cases bag and mask support of ventilation may be needed). • Assess/monitor circulation and obtain IV access: • Fluid resuscitation may be needed to restore BP • Rapidly assess consciousness level and confirm presence of seizure. • Obtain a brief history. • Administer first-line antiseizure therapy: lorazepam IV 4 mg bolus: • Use diazepam IV (or rectally) 10 mg if lorazepam unavailable • Alternatively: midazolam 10 mg to buccal mucosa, or 200 mcg/kg intranasally (unlicensed alternative to lorazepam) • Within ICU a 2–4-mg bolus of midazolam may be used as first-line therapy if an infusion is already running • If there is no response after 5 minutes dose can be repeated (with monitoring of pulse oximetry and respiration). Further seizure assessment and control: • Perform finger-prick blood sugar test, if hypoglycaemic, give 50 ml of 50% glucose IV or 500 ml 10% glucose (the need for hypoglycaemia correction outweighs the risk of exacerbating cerebral ischaemia). • If alcoholism, or malnourishment, is suspected give thiamine 250 mg (Pabrinex® 2 ampoules) IV over 10 minutes. • In women of child-bearing age perform a pregnancy test: if eclampsia is suspected follow protocol (b p.432, magnesium sulphate, loading dose: 20 mmol/4g IV over 3–5 minutes, followed by maintenance infusion of 5–10 mmol/hour).

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• If seizure activity persists despite initial therapy commence second-line therapy: phenytoin (in 0.9% saline) 18 mg/kg IV infusion at a rate not exceeding 50 mg/minute; ECG monitoring is required: 1 • Alternatively use fosphenytoin, 15mg(P.E. )/kg IV infusion (maximum rate 100–150mg(P.E.1)/minute); ECG monitoring required • In patients known to be on regular phenytoin avoid loading dose but consider using maintenance dose. If seizure activity persists 20 minutes from first presentation (or if the patient is severely hypoxic, acidotic or hypotensive at any time): • Induce general anaesthesia using thiopental or propofol, as a rapid sequence intubation with suxamethonium (or rocuronium if serum potassium is high). • Sedate with propofol or midazolam infusions (both may be required). • Avoid further muscle relaxant infusions unless absolutely necessary (may mask further seizures). • EEG monitoring must be used if muscle relaxant infusions are used (e.g. atracurium infusions). • If seizures persist discuss diagnosis and treatment with neurology: • Possible treatments include: levetiracetam (500–1000 mg IV), sodium valproate (800 mg IV over 3–5 minutes), lacosamide (50 mg IV BD over 15–60 minutes), or the addition of thiopental 1–5 mg/kg/hour IV or phenobarbital 5–12 mg/kg IV (maximum rate 100 mg/minute); follow-up doses of antiepileptics should be discussed with a neurologist • EEG/CFAM monitoring should be organized, aiming for a burst suppression pattern 1

Phenytoin equivalents (P.E.) are used for fosphenytoin: fosphenytoin 1.5 mg = phenytoin 1 mg.

Further management • Perform a head CT if required (b p.155). • Ensure that a full neurological assessment has been carried out and discuss the case with a neurologist. • Maintain PaCO2 4.5–5 kPa, PaO2 10 kPa, temperature 37°C, Hb 10 g/dl, glucose 6–10 mmol/L, serum Na 135–140 mmol/L, where possible. • If ICP monitoring in place, maintain ICP 65 mmHg. • Where there is evidence of hypotension commence fluid resuscitation with inotropic support if required. • Other complications which may require treatment include: cerebral oedema (b p.186), neurogenic pulmonary oedema (b p.86), aspiration (b p.66), lactic acidosis (b p.204), electrolyte disturbances, rhabdomyolysis and acute renal failure (b p.268), DIC (b p.306).

Pitfalls/difficult situations • If seizure control is achieved reassess airway as the sedative effects of treatment may require endotracheal intubation/ventilation. • Many drugs lower the fit threshold (e.g. flumazenil and antipsychotics).

SEIZURES AND STATUS EPILEPTICUS

• Status epilepticus is not common in epileptics; always consider other causes of seizures such as infections. • Psychogenic seizures may be superficially similar to convulsive status epilepticus; the diagnosis is supported by the absence of hypoxia or acidosis, and if suspected a neurology opinion should be sought. • Where tumour or vasculitis are present consider dexamethasone. • Valproate may be preferred as second-line therapy for absence states.

Patients with generalised tonic-clonic status epilepticus

11 10 9 8 7

12

D 1 2 3 4

6

5

immediate measures

secure airway give oxygen assess cardiac and respiratory function secure intravenous (IV) access in large veins collect blood for bedside blood glucose monitoring and full blood count, urea and electrolytes, liver function tests, calcium, glucose, clotting, AED levels and storage for later analyses measure blood gased to extent of acidosis

A give lorazepam 4mg IV (or diazepam 10mg IV if lorazepam is unavailable) no response?

delay in IV access in community?

repeat after maximum of 10 minutes if in hospital

give 10–20mg diazepam rectally

D Determine aetiology: any suggestion of hypoglycaemia: give 50ml 50% glucose IV any suggestion of alcohol abuse or impaired nutritional status: give thiamine IV (as 2 pairs of ampoules Pabrinex ®) give usual AED treatment orally or by nasogastric tube (or IV if necessary for phenytoin, sodium valproate and phenobarbital) 11 10 9 8 7

12

if status persists

1 2 3 4

6

B

5

within 30 minutes 11 10 9 8 7

12

2 3 4 6

D

1

5

>30 minutes

give fosphenytoin 18mg/kg phentoin equivalent IV, up to 150mg/min; or phenytoin 15mg/kg IV, 50mg/ min both with ECG monitoring; or phenobarbital 15mg/kg IV, 100mg/min call ITU to inform of patient if status persists

D

administer general anaesthesia and admit to ITU monitor using EEG to assess seizure control refer for specialist advice

Fig. 5.1 Algorithm for the management of status epilepticus, SIGN (2003). Reproduced with permission from Scottish Intercollegiate Guidelines Network.

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Further reading Costello DJ, et al. Treatment of acute seizures and status epilepticus. J Intensive Care Med 2007; 22: 319–47. Meierkord H, et al. EFNS guideline on the management of status epilepticus in adults. Eur J Neurol 2010; 17: 348–55. Maganti R, et al. Nonconvulsive status epilepticus. Epilepsy Behav 2008; 12: 572–86. NICE. The epilepsies: the diagnosis and management of the epilepsies in adults and children in primary and secondary care. London: NICE, 2012. Rossetti AO, et al. Management of refractory status epilepticus in adults: still more questions than answers. Lancet Neurol 2011; 10: 922–30. Scottish Intercollegiate Guidelines Network. Diagnosis and management of epilepsy in adults. A national clinical guideline. Edinburgh: SIGN, 2003.

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2 Stroke/thromboembolic stroke A stroke (sometimes called a cerebrovascular accident, CVA, or occasionally a ‘brain attack’) is defined as an acute focal neurological deficit caused by cerebrovascular disease that lasts >24 hours or causes death. If the focal neurological deficit lasts 70%). • ECHO (the source of any emboli may be cardiac). • Other investigation that may be of benefit include: • CRP, ESR • Thrombophilia screen • Auto-antibody screen • Plasma electrophoresis • Blood cultures • Syphilis screen • • • • • • • •

Differential diagnoses • • • • • •

Migraine. Hypoglycaemia. Partial epileptic seizures, or following seizures (post-ictal states). Space-occupying lesions (e.g. tumour, abscess or subdural haematoma). Demyelinating disease. Cerebral venous thrombosis.

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Immediate management • Titrate O2 to achieve SpO2 >94% (O2 may not be required). • Airway may be compromised due to impaired conscious level, place patient in recovery position or intubate trachea as appropriate. • Few stroke patients benefit from invasive ventilatory support but some might if gag reflex is absent, the GCS is 94%. • Airway may be compromised due to impaired conscious level, place the patient in recovery position or intubate trachea as appropriate.

INTRACEREBRAL HAEMORRHAGE

• Ensure breathing/ventilation is adequate: • Avoid hypercapnia • Avoid hyperventilation and hypocapnia unless required for short periods (3 cm, or occluding the 4 ventricle • A supratentorial haemorrhage of 20–80 ml volume causes GCS >4 and 60 mmHg where appropriate. • Manage intracranial hypertension as appropriate (b p.186). • Maintain blood glucose at 6–10 mmol/L.

Pitfalls/difficult situations (See b p.169.) • It is difficult to clinically distinguish between ischaemic stroke and ICH, early CT scan will show ICH, but may not show ischaemic strokes. • Neurosurgery is unlikely to benefit those patients who have: GCS 12 with small haemorrhages, brainstem haemorrhage, significant comorbidity (or who are elderly). • Up to 5% of patients have a recurrent ICH, risk factors for recurrence include: uncontrolled hypertension, lobar location of initial ICH, older age, ongoing anticoagulation, apolipoprotein E epsilon 2 or epsilon 4 alleles, large number of microbleeds on MRI.

Further reading Hemphill JC et al. The ICH score: a simple, reliable grading scale for intracerebral haemorrhage. Stroke 2001; 32(4): 891–7. Mendelow AD, et al. Surgical treatment of intracerebral haemorrhage. Curr Opin Crit Care 2007; 13(2): 169–74. Morgernstern LB, et al. Guidelines for the management of spontaneous intracerebral haemorrhage AHA/ASA Guideline. Stroke. 2010; 41(9): 2108–29.

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3 Subarachnoid haemorrhage Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space and not into the brain parenchyma itself. It accounts for up to 7% of strokes with an incidence of 6–8:100,000. 50% of patients with SAH will die, 12% before reaching hospital. 20% will have multiple aneurysms.

Causes Risk factors for spontaneous (non-traumatic) SAH include: • Hypertension/malignant hypertension. • Diabetes and/or hyperlipidaemia. • Smoking. • Migraine. • Drug abuse (particularly cocaine). • Family history (first-degree relatives have a 2–5-fold increase of risk). • Female to male ratio is 2:1; black/Afro-Caribbean > white/Caucasian. • Associated with syndromes (Marfan’s, Ehlers–Danlos, Klinefelter’s). • Associated with polycystic kidney disease and coarctation of the aorta. Saccular (berry) aneurysms account for 80% (often occurring at cerebral vessel junctions); the larger the aneurysm, the higher the risk of rupture. Other causes include: • Non-aneurysmal perimesencephalic haemorrhage. • Arterial dissection; cerebral or dural arteriovenous malformations; vascular lesions of the spinal cord; cerebral venous thrombosis . • Mycotic aneurysms. • Sickle cell disease. • Pituitary apoplexy. • Cerebral amyloid.

Presentation and assessment Patients can present with symptoms ranging from ‘the worst headache in my life’ to coma. Patients needing critical care commonly present with: • Airway/respiratory: grunting, snoring, or obstruction; Cheyne–Stokes breathing, tachypnoea, bradypnoea (hypoventilation occurs late): • Neurogenic pulmonary oedema may sometimes occur • Cardiovascular changes: tachycardia and/or hypertension (hypertension associated with bradycardia is a late or pre-terminal sign): • ECG changes associated with ischaemia can occur Neurological signs and symptoms may include: • Headache (SAH accounts for 78% of headaches presenting to A&E): • Classically a sudden-onset (peaks within minutes), worst-ever, ‘thunderclap’ headache, often occipital (as if ‘hit from behind’) • Any severe headache may be suspicious, particularly in patients who do not usually suffer headaches • Some patients describe recent minor headaches (sentinel bleeds) • Meningism: nausea and vomiting, photophobia, neck stiffness. • Diminished consciousness, or loss of consciousness. • Focal neurological signs and/or seizures. • Signs of raised ICP may be present (see b p.186).

SUBARACHNOID HAEMORRHAGE

World Federation of Neurological Surgeons (WFNS) grading of subarachnoid haemorrhage1 I

GCS 15

Conscious with/without meningism No motor deficit II GCS 14–13 Drowsy with no significant neurological deficit No motor deficit III GCS 14–13 Drowsy with neurological deficit Motor deficit present or absent IV GCS 12–7 Deteriorating patient Major neurological deficit Motor deficit present or absent V GCS 3–6 Moribund patient with extensor rigidity Failing vital centres Motor deficit present or absent. The grade, extent of haemorrhage on CT scan, combined with patient age can be used to estimate prognosis. Other grading scales include Hunt and Hess, and the Fisher scale (radiological scale). 1

Reproduced from Journal of Neurology, Neurosurgery and Psychiatry, G.M. Teasdale, 51, 11, pp. 1457, copyright 1988, with permission from BMJ Publishing Group Ltd.

Investigations ABGs (to exclude hypoxia and hypercapnia). FBC, coagulation studies. U&Es (salt wasting can be present), LFTs. Serum glucose, serum magnesium (hypomagnesaemia is common). ECG (arrhythmias, ischaemia, and infarcts are common). CXR (may identify pulmonary oedema). Initial CT head (to clarify diagnosis, extent of cerebral damage, differentiate infarct from haemorrhage and exclude hydrocephalus); CT scans done within the first 24 hours have a sensitivity of 95–98%: • CT angiogram can identify aneurysm and is the gold standard in centres where this service is available • Initially negative angiography should be repeated as up to 24% of vascular lesions are identified on repeat angiography • LP if CT head is negative (may identify xanthochromia): • Sequential collection of CSF with RBC count shows no reduction in RBC in all 3–4 bottles collected (not always reliable) • Xanthochromia may not be present until at least 6–12 hours after episode (as blood has to lyse in CSF) • Opening pressure protein and glucose should also be measured • CSF should also be examined to exclude meningitis (b p.574). • • • • • • •

Differential diagnoses Meningitis, encephalitis (the major differential diagnosis). Migraine, cluster and thunderclap headaches. Postdural puncture headache. Subdural/extradural haemorrhage; ischaemic stroke, intracerebral haemorrhage; acute hydrocephalus. • Temporal arteritis. • • • •

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Immediate management • Give 100% O2 initially, then titrate to achieve SpO2 >94%. • Airway/breathing may be compromised due to impaired conscious level, this may require endotracheal intubation/mechanical ventilation: • Avoid hypercapnia (maintain PaCO2 4.5–5 kPa) • Avoid hyperventilation/hypocapnia unless required for short periods (150mmol/L, hypertonic saline and mannitol are contraindicated). LFTs. Consider blood alcohol levels and other drug levels where appropriate (e.g. paracetamol and salicylate). ECG (ischaemic changes may be present). Trauma X-rays (C-spine, CXR, pelvis). CT scan head and neck (see indications b p.155): ideally should be done within 10 minutes of arrival in hospital and be reported within 1 hour.

Differential diagnoses • • • •

Stroke. Meningitis, encephalitis. Subarachnoid haemorrhage. Intoxication (alcohol or drugs); overdose.

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Immediate management • Give 100% O2 and support airway, breathing, and circulation as required (see rest of box), maintain SaO2 >94%. • Use spinal precautions including hard collar, sand bags, and strapping (and in-line manual stabilization for intubation). • Obtain a contemporaneous history if possible (e.g. from relatives or ambulance crew); an ‘AMPLE’ history (b p.2) should be obtained as a minimum. • Roughly assess neurological state (e.g. conscious and talking, level of consciousness, or lateralizing signs) and simultaneously treat neurological complications which may interfere with ABC (e.g. seizures). • Complete basic ABC p survey before formally assessing neurological state. Airway • Airway may be compromised due to impaired conscious level, intubate the trachea as appropriate (placement of the patient in the recovery position is likely to be contraindicated by the need for spinal precautions). • If endotracheal intubation is needed a rapid sequence intubation will be required to minimize the risk of aspiration; the hard collar will need to be undone, and manual in-line stabilization used in its place. • Rapid sequence endotracheal intubation should be considered if: • GCS 8 (severe head injury), or rapidly deteriorating • There is risk of aspiration of vomit or blood • There is facial or neck trauma putting the airway at risk • There is evidence of hypoxia (SaO2 5 kPa) or marked tachypnoea • Short-term deliberate hyperventilation is required • There is ongoing seizure activity • The patient is unlikely to remain still for investigations (e.g. CT) • The patient is agitated and combative but requiring treatment • Endotracheal intubation may be required to manage thoracic trauma resulting in respiratory compromise (see b p.80, 82 and 410). • Any stress response to endotracheal intubation should be avoided if possible; IV induction and sedation will help avoid rises in ICP, and opioids should be given as part of the induction: • Muscle relaxants may be required for stabilization or transfer, but may mask seizures. Breathing • Ensure breathing/ventilation is adequate: • Ventilatory support may be needed to optimize oxygenation, avoid hypoxia aiming for a PaO2 >10 kPa • Avoid hypercapnia (aim for PaCO2 4.5–5 kPa) • Avoid hyperventilation and hypocapnia unless required for short periods (90 mmHg, whichever is higher). • Resuscitate with fluids and blood as required, use normal saline preferentially and avoid hypotonic fluids (dextrose containing fluids); inotropes may be required after normovolaemia is established. Neurology • Further useful history may include: • History of significant period of amnesia, or loss of consciousness • Mechanism of injury in trauma cases • Formally assess neurological status, including: • GCS (see b p.153) • Eye examination including pupil size and reactivity, and fundoscopy if possible • Evidence of vault or base-of-skull fracture (otoscopy is required) • Plantar reflexes • Reassess GCS once airway, breathing, and circulation have been stabilized, and continue to regularly reassess consciousness and neurological state. Other • Exclude and treat hypoglycaemia and hypothermia. • Urgent CT scan may be required for diagnosis and appropriate management (prevent hypoxia, hypercapnia, hypotension, and hypertension throughout): • Patients should be stabilized for transfer prior to CT scan • Raised ICP may be treated with mannitol (0.5–1 g/kg IV) or hypertonic saline (if serum sodium is 90 mmHg should ensure an acceptable CPP • Later MAP may be guided by ICP or other measurements (maintaining CPP of >60–65 mmHg) • Fluid resuscitation aiming for euvolaemia (avoiding albumin, and hypotonic fluids where possible) may be sufficient, though inotropes may be needed • Monitor urine output. Neurological • If not intubated/ventilated, perform regular neurological observations: • If intubated and ventilated then pupillary reflexes should be observed and it would be prudent for an ICP bolt to be inserted • Sedatives with rapid offset such as propofol may initially be advisable as it will allow level of consciousness to be easily reassessed. • Heavy sedation may be required to avoid coughing and gagging on the ETT (which might raise ICP); occasionally thiopental coma will be used as a final attempt at medical management of high ICP. • Muscle relaxants may be required for the initial intubation, stabilization, or transfer, but may mask fitting: • Where muscle relaxants are used consider concurrent antiepileptic sedative infusions (such as propofol or midazolam) and/or loading with anticonvulsants • In uncontrolled intracranial hypertension where patients are receiving muscle relaxants, CFAM should be used and burst suppression of 10% should be achieved • A 15–30° head-up tilt will aid cerebral venous drainage (where spinal precautions are in place the whole bed may be tilted). • Where ICP is measured it should be kept 20 mmHg (see b p.186): • Cerebral perfusion pressure (CPP) should be maintained at 60–65 mmHg (CPP = MAP − ICP) • Hypothermia of no less than 35°C can be used to control severe intracranial pressure • Hypertonic saline has been used as a means to increase serum sodium and treat resistant high ICP • Some neurosurgical centres will perform decompressive craniectomy on patients who fail medical therapy (this is currently controversial and awaiting the outcome from further studies) • Transcranial Doppler (TCD) monitoring may identify vasospasm.

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• Consider seizure prophylaxis using phenytoin 15 mg/kg bolus then 300 mg daily IV/NG. • Where seizures are witnessed or suspected, treat aggressively with antiepileptic drugs such as phenytoin. • Further head CTs may be indicated if there is any change in GCS, pupil, or neurological signs. • Polyuria may indicate hypothalamic injury causing diabetes insipidus (incidence 40%); or the use of osmotic diuretics.

Indications for considering ICP measurement • Severe head injury (GCS 135 mmol/L. •

Pitfalls/difficult situations • There may be a lucid interval between the initial head injury and the development of an intracranial haematoma; close monitoring is advisable for 4–6 hours after serious injuries. • In some cases general surgical interventions (e.g. for major internal haemorrhage) may take precedence over investigating or treating neurological problems.

Indicators of poor prognosis • • • • •

GCS 3–7. Fixed, dilated pupils. Hypotension (systolic < 90 mmHg). Age >60 years. CT scan findings: • Blood in the basal cisterns • Traumatic SAH • Midline shift • Intracerebral mass lesions

Data from the Brain Trauma Foundation guidelines, ‘Early Indicators of Prognosis in Severe Traumatic Brain Injury’. M https://www.braintrauma.org/pdf/protected/prognosis_guidelines.pdf

Further reading Brain Trauma Foundation website: M. Cooper DJ, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011; 364: 1493–502. Girling K. Management of head injury in the intensive-care unit. Cont Educ Anaesth Crit Care Pain 2004; 4(2): 52–6. NICE. Head injury. Triage, assessment, investigation and early management of head injury in infants, children and adults. London: NICE, 2007. Leal-Noval SR, et al. Optimal hemoglobin concentration in patients with subarachnoid hemorrhage, acute ischemic stroke and traumatic brain injury. Curr Opin Crit Care 2008; 14(2): 156–62. Morris C, et al. Evaluation for spinal injuries among unconscious victims of blunt polytrauma: A management guideline for intensive care. London: Intensive Care Society, 2005. SAFE study Investigators. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med 2007; 357: 874–84. Vergouwen MDI, et al. Venous thromboembolism prophylaxis and treatment in patients with acute stroke and traumatic brain injury. Curr Opin Crit Care 2008; 14(2):149–55.

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4 Raised intracranial pressure ICP is the pressure of the brain parenchyma, CSF, and blood (venous and arterial) inside a rigid skull. Normal ICP is 0–10 mmHg. Raised ICP occurs when compensatory mechanisms to reduce ICP fail, and is defined as 20 mmHg for >5 minutes. Management aims to maintain CPP 60 mmHg. CPP = MAP – ICP.

Causes1 • Space-occupying lesions, including neoplasm, abscess, or haematomas. • Vasogenic cerebral oedema: TBI, infection, hepatic encephalopathy, eclampsia, hypertensive encephalopathy, sinus thrombosis, altitude cerebral oedema. • Cytotoxic oedema: post-cardiac arrest, acute hyponatraemia. • Interstitial oedema: hydrocephalus. • Idiopathic intracranial hypertension. Certain patients are at higher risk of developing raised ICP: following TBI; following neurosurgery (especially where haemostasis is poor); younger patients (compared with older patients).

Presentation and assessment Within the ICU, raised ICP is most often identified as a result of ICP monitoring, or intraventricular drain, showing • ipressures, or abnormal waveforms (normal ICP waves resemble arterial pressure waveforms, waveforms affected by raised ICP often have the highest peak after the dicrotic notch). Clinical signs and symptoms of raised ICP are those associated with dconsciousness (b p.152) and any underlying cause, e.g. head injury (b p.178), SAH (b p.174), stroke (b p.166). They may include: • Listlessness, irritability, headache, vomiting. • Pupils: unequal, sluggish or divergent; papilloedema on fundoscopy. • Seizures or focal neurological signs. • Hypertension, bradycardia; Cheyne–Stokes respiration.

Investigations • • • •

ABGs (to assess PaCO2), FBC, coagulation studies. U&Es, LFTs; serum osmolality and glucose. Core temperature. CT head is essential if raised ICP is suspected in an unmonitored patient; consider CT head if there is an acute rise in monitored ICP.

Differential diagnoses • Where no monitoring is present: SAH, meningitis/encephalitis, migraine, stroke. • Where ICP monitoring is present: incorrect calibration of probe.

1 ICP monitoring is most frequently done for TBI. Management algorithms for other conditions are often extrapolated from evidence for TBI.

RAISED INTRACRANIAL PRESSURE

Immediate management: In new patients with suspected raised ICP identify/treat the acute cause: • Give 100% O2; support airway, breathing, and circulation as required. • Patients with raised ICP may need intubation/ventilation prior to CT. Where ICP is shown to be raised in an already intubated ICU patient: • Check transducers for errors if ICP is monitored. • Ensure adequate analgesia (also ensuring urinary catheter is patent) and sedation; consider neuromuscular blockade after sedation. • Tilt patient up to 30° head up; ensure neck veins not obstructed. • Maintain PaCO2 4.5–5 kPa and PaO2 10 kPa; monitor ABG/ETCO2. • Aim for a CPP 60 mmHg using inotropes/vasopressors (after achieving euvolaemia) ensuring a MAP of 80–90 mmHg. • Avoid treating hypertension unless MAP >130 mmHg; use short-acting antihypertensives (e.g. esmolol) aiming for 20% reduction. • Give mannitol 20%, 0.5–1 g/kg over 15 minutes (repeat up to 4-hourly; stop if plasma osmolality 320 mOsmol/L or sodium >155 mmol/L). • Keep core temperature 37°C with surface cooling and paracetamol. If ICP fails to reduce or continues to increase the following may help: • Repeat CT head to identify new treatable case. • Hypertonic saline infusion, further mannitol, or furosemide 20–40 mg. • Thiopentone 75-mg boluses, or a thiopentone infusion. • Inducing moderate hypothermia (34–35°C). • Moderate hyperventilation to PaCO2 38.5ºC) and often hyperpyrexia (>40ºC): • Sweating, fatigue • Cardiovascular: hypertension followed by hypotension: • Sinus tachycardia >140 beats/minute (often disproportionate to degree of fever) • AF, multifocal ventricular ectopics • Angina • Cardiac failure (30% of cases); typically high-output cardiac failure • Respiratory: tachypnoea, dyspnoea: • If already ventilated: failure to wean, ‘fighting’ the ventilator • Neurological: agitation, delirium, aggression, seizures, coma: • Hyporeflexia and myopathy are occasionally present • GI: anorexia, weight loss: • Abdominal pain • Nausea, vomiting, diarrhoea • Hepatic failure, jaundice • Renal failure (s to rhabdomyolysis).

Investigations Diagnosis is clinically based; no laboratory tests are diagnostic; a scoring system is available which may assist in making the diagnosis (Table 6.2). Do not delay treatment whilst awaiting lab results: • TFTs: T3, free T4 and TSH (elevated T4/T3, suppressed TSH). • ABGs (respiratory failure, metabolic acidosis). • FBC (raised WCC).

THYROID STORM

U&Es (hyperkalaemia). LFTs (raised transaminases and bilirubin). Serum calcium (hypercalcaemia). Serum magnesium (hypomagnesaemia). Serum CK (rhabdomyolysis may occur). Serum glucose (may be d). Blood, sputum and urine cultures (if infection suspected). Urinary myoglobin, urinary catecholamines (to exclude differential diagnoses). • ECG (myocardial ischaemia/MI, arrhythmias, LV hypertrophy). • CXR (if pulmonary oedema or pneumonia suspected). • CT head (if intracranial pathology/infection needs to be excluded). • • • • • • • •

Differential diagnoses • • • • • • • •

Malignant hyperpyrexia. Phaeochromocytoma. Serotonergic syndrome. Infection/sepsis. Anticholinergic or adrenergic drug intoxication. LVF/CCF. Hyperthyroidism, without thyroid storm. Essential hypertension.

Immediate management • Give O2 and support airway, breathing, and circulation as required. Symptom control is the priority, rather than correcting thyroid status: • Do not await lab test confirmation of suspected diagnosis. • Protect and support airway and breathing as required; relative hyperventilation is required to compensate for hypermetabolic state. • Circulatory support with IV saline 0.9% may be required in view of large insensible losses from hyperpyrexia, diarrhoea, and vomiting: • ECG monitoring is required • Replace glucose as required. • Hyperpyrexia (see also b pp.246 and 248) employ cooling measures: • Tepid sponging, axillae/femoral ice packs, cooling blankets • Peritoneal or NG lavage with ice cold fluid may be used • Haemofiltration or endovascular temperature-therapy catheter • Antipyretics: IV paracetamol 1g 6-hourly—do not use NSAIDs or other drugs which displace thyroid hormone from binding sites • Consider dantrolene as T4 causes calcium release similar to malignant hyperpyrexia (see b p.246) • Hyperadrenergic state: • Propranolol 1–5 mg IV up to 10 mg (can precipitate CCF); aim for pulse rate 45 suggestive of thyroid storm Temperature (ºC)

Score

37.0–37.7

5

37.8–38.2

10

38.3–38.7

15

38.9–39.3

20

39.4–40.0

25

>40.0

30

CNS effects Absent

0

Agitation

10

Delirium, psychosis, extreme lethargy

20

Seizure, coma

30

GI or hepatic symptoms Absent

0

Diarrhoea, abdominal pain, nausea and vomiting

10

Jaundice

20

Tachycardia (beats/minute) 90–109

5

110–119

10

120–129

15

130–139

20

t140

25

Atrial fibrillation Absent

0

Present

10

Heart failure Absent Mild (pedal oedema)

0 5

Moderate (bibasal crepitation)

10

Severe (pulmonary oedema)

20

Precipitant history Absent

0

Present

10

This information is adapted from Endocrinology and Metabolism Clinics of North America, 22, 2, Burch HB, et al. ‘Life-threatening thyrotoxicosis. Thyroid storm.’, pp. 263–277, Copyright Elsevier 1993.

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Further reading Migneco A. et al. Management of thyrotoxic crisis. Eur Rev Med Pharmacol Sci 2005; 9(1): 69–74. Nayak B, et al. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am 2006; 35: 663–86. Petry J, et al. Plasmapheresis as effective treatment for thyrotoxic storm after sleeve pneumonectomy. Ann Thorac Surg 2004; 77: 1839–41.

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3 Phaeochromocytoma and carcinoid syndrome Phaeochromocytomas are catecholamine-producing tumours, which may present acutely, or coincidentally with another condition. Carcinoid syndrome is a collection of features caused by a carcinoid tumour secreting serotonin, 5-hydroxytryptophan, and other mediators.

Causes Phaeochromocytomas may present in isolation (10% malignant, 10% bilateral, 10% familial, 10% extra-adrenal) or as part of a syndrome: MEN 2a/b, von Recklinghausen’s disease and von Hippel–Lindau disease. Carcinoid tumours are found in stomach, bowel, pancreas, or bronchus. Factors that provoke release of mediators include tumour manipulation, catecholamine use, or the presence of liver metastases.

Presentation and assessment Phaeochromocytoma Signs/symptoms are more likely to manifest after painful procedures such as: endotracheal intubation or direct tumour manipulation; they are due to excessive sympathetic activity. • General: anxiety, tremor, weakness, faintness, paraesthesia, cold extremities, pallor, drenching perspiration. • Cardiovascular: hypertension (sustained or paroxysmal): • Myocardial ischaemia, palpitations, tachycardia, AF or VF • Metabolic: unexplained lactic acidosis. Carcinoid syndrome Features vary in severity and depend upon the tumour location and subtype. Pre-existing features may include: cardiac valve abnormalities (TR), pulmonary stenosis and right heart failure. Features related to secretion of vasoactive substances include: • General: flushing, nausea/vomiting, abdominal pain, diarrhoea, hyperglycaemia. • CVS/RS: vasodilatation, hypotension, SVT, bronchoconstriction: • Haemoptysis and airway obstruction (in bronchial carcinoid)

Investigations ABGs (metabolic acidosis). U&Es (hypokalaemia, iurea in phaeochromocytoma). Glucose (hyperglycaemia). ECG (arrhythmias, LVH in phaeochromocytoma, RVH in carcinoid). CXR (pulmonary metastases in carcinoid). CT scan/US abdomen (to locate tumours/liver metastases). Phaeochromocytoma: 24-hour urine collection for VMA, catecholamines and metanephrine levels, and/or plasma catecholamines (if available): • Pentolinium suppression test (suppression will occur) • Carcinoid: serum levels for of serotonin and/or 5 hydroxytryptophan: • Urine for 5 hydroxyindoleacetic (5HIAA) acid levels • • • • • • •

PHAEOCHROMOCYTOMA AND CARCINOID SYNDROME

Differential diagnoses • Essential hypertension; inadequate sedation, analgesia, or anaesthesia. • Hypertensive diseases: pre-eclampsia, thyroid storm. • Inadvertent vasopressor bolus; or administration of indirect acting vasopressors (e.g. ephedrine) to patients taking MAOIs. • Bronchospasm (e.g. anaphylaxis, asthma).

Immediate management • Give O2 and support airway, breathing, and circulation as required. • Stop any avoidable stimulus, deepen any anaesthesia/sedation. • Invasive monitoring if cardiovascularly unstable (arterial line, CVC). Suspected phaeochromocytoma (adrenergic control) • Sole β-blockade may precipitate a hypertensive crisis due to unopposed alpha receptor stimulation. • Give phentolamine (non-selective α-blocker) 2–5 mg IV bolus and repeat as necessary to control hypertension: • Alternatively doxazosin PO 2–4 mg/day • If further hypertensive control is required consider: • Magnesium sulphate 5 g (20 mmol) IV then 2 g/hour (8 mmol) • Sodium nitroprusside IV 0.5–1.5 mcg/kg/minute • After alpha blockade established if HR >100 beats/minute, or there are frequent VEs, consider: • Labetalol 5–10 mg IV increments, or esmolol 1.5 mg/kg bolus IV Suspected carcinoid • Give nebulized ipratropium bromide 500 mcg and IV/inhalational steroids for bronchospasm (avoid β agonists). • Commence fluid resuscitation for hypotension. • Use phenylephrine 50–100 mcg boluses/IVI (can be given via a peripheral vein) for refractory hypotension. • Give octreotide 50–100 mcg IV (this drug prevents the release, and block the peripheral actions of serotonin and other mediators).

Further management • Phaeochromocytoma: stabilize on antihypertensive regimen: • The definitive treatment is excision of the p tumour • Carcinoid: correct any electrolyte abnormalities: • Avoid hypoxia or hypercapnia which can increase mediator release.

Pitfalls/difficult situations • • • •

The diagnosis is frequently not straightforward. The presence of RVF may complicate management of carcinoid. Phaeochromocytoma causes hypovolaemia masked by hypertension. Other endocrine abnormalities (e.g. Cushing’s syndrome) may coexist.

Further reading Kulke MH, et al. Carcinoid tumors. N Engl J Med 1999; 340: 858–68. Nguyen-Martin MA, et al. Phaeochromocytoma: an update on risk groups, diagnosis and management. Hosp Physician 2006; Feb: 17–24.

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4 Malignant hyperpyrexia and neurolept malignant syndrome Malignant hyperpyrexia (MH) is an inherited disorder, which in susceptible individuals exposed to triggering agents causes intense muscle activity and a hypermetabolic state. Triggering agents are mostly used during anaesthesia, but critical care is required for on-going management. Neurolept malignant syndrome (NMS) is a potentially fatal, idiosyncratic response to neuroleptic drugs and tranquillizers.

Causes • MH: • Suxamethonium or volatile anaesthetic agents (e.g. isoflurane) • NMS: • Caused by: phenothiazines, butyrophenones, thioxanthenes, lithium • May be triggered by exercise, exhaustion, or dehydration Presentation and assessment (See Boxes 6.1 and 6.2.) • Muscle rigidity (or masseter spasm) and akinesia; metabolic acidosis. • Rapid rise in core body temperature; sweating. • Tachycardia, arrhythmias, autonomic impairment (labile BP). • Complications of hyperpyrexia (see b p.248). Investigations (See also b p.248.) • ABGs (acidosis, hypercapnia, low bicarbonate, hypoxia). • FBC (iWCC/platelets in NMS; thrombocytopaenia in DIC). • Coagulation screen (iPT/APTT, dfibrinogen in DIC). • U&Es (hyperkalaemia, raised urea/creatinine). • CK (raised in rhabdomyolysis); LFTs (may be deranged). • Serum phosphate (may be raised), serum calcium (may be low). • TFTs (to exclude the differential of hyperthyroidism). • Blood, urine and sputum cultures (if infection suspected). • Urine (for toxicology and/or myoglobinuria). • ECG (if ischaemia is suspected), CXR (if infection suspected). • Consider CT scan or lumbar puncture (if focal infection suspected).

Differential diagnoses • Diseases associated with hyperthermia (e.g. sepsis, heat stroke). • Diseases associated with rigidity (e.g. tetanus, Parkinson’s disease).

Box 6.1 Management of a malignant hyperthermia crisis Know where dantrolene is stored. Recognition • Unexplained increase in ETCO2 and unexplained tachycardia and unexplained increase in O2 requirement. • Temperature changes are a late sign. Immediate management 1. Stop all trigger agents, call for help. 2. Allocate specific tasks (use an action plan if available). 3. Use a new breathing circuit/system and hyperventilate 100% O2.

MH AND NMS

4. Maintain anaesthesia with an intravenous agent. 5. Abandon/finish surgery as soon as possible. 6. Any muscle relaxation should be with a non-depolarizing neuromuscular blocking drug (e.g. atracurium). 7. Give dantrolene and initiate active cooling (avoid vasoconstriction). Monitoring and treatment • Dantrolene: 2.5 mg/kg IV bolus; repeat 1-mg/kg boluses as required to 10 mg/kg maximum (for a 70-kg adult: initial bolus of 9 dantrolene vials, each 20-mg vial mixed with 60 ml H2O; further boluses of 4 vials dantrolene repeated up to 7 times). • Hyperkalaemia: calcium chloride, glucose/insulin, NaHCO3. • Arrhythmias: magnesium/amiodarone/metoprolol. • Avoid calcium channel blockers (interacts with dantrolene) • Metabolic acidosis: hyperventilate, NaHCO3. • Myoglobinaemia: urinary alkalinization, may require RRT later. • DIC: FFP, cryoprecipitate, platelets. • Check serum CK as soon as possible. • Continuous monitoring: core and peripheral temperature, SpO2, ETCO2, invasive BP, ECG, CVP. • Repeated blood tests: ABGs, U&Es (potassium), FBC (haematocrit/ platelets), coagulation studies. Follow-up • Continue monitoring on ICU, repeat dantrolene as necessary. • Monitor for acute kidney injury and compartment syndrome. • Repeat CK. • Consider alternative diagnoses (sepsis, phaeochromocytoma, thyroid storm, myopathy). • Counsel patient and family members; refer to an MH unit1. 1

The UK MH Investigation Unit, Academic Unit of Anaesthesia, Clinical Sciences Building, Leeds Teaching Hospitals NHS Trust, Leeds LS9 7TF. Direct line: 0113 206 5270. Fax: 0113 206 4140. Emergency Hotline: 07947 609601. Reproduced with the kind permission of the Association of Anaesthestists of Great Britain and Ireland.

Box 6.2 Management of neurolept malignant syndrome • Stop causative agents. • Supportive management/cooling as in hyperthermia (see b p.248). • Consider the following drug therapy: dantrolene (use MH guidelines), diazepam, levodopa (orally), bromocriptine, amantadine.

Further management • Repeat drug therapy if required. • Continue monitoring and support therapy for at least 72 hours. • Otherwise follow management plan for hyperpyrexia (see b p.249).

Further reading Adnet P, et al. Neuroleptic malignant syndrome. Br J Anaesth 2000; 85(1): 129–35. Glahn KPE, et al. Recognizing and managing a malignant hyperthermia crisis: guidelines from the European Malignant Hyperthermia Group. Br J Anaesthesia 2010; 105(4): 417–20. AAGBI/British MH Association. Malignant hyperthermia crisis. London: AAGBI, 2011.

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3 Hyperthermia and heat injury • Hyperthermia is defined as a core body temperature >38oC. • Severe hyperthermia is >40.5oC sustained for >1 hour. At >42oC cellular enzymes cease to function, proteins are denatured, and there is extensive damage to endothelium, nervous tissue and the liver.

Causes Factors that increase body heat production, or ddissipation: • Environmental exposure (heat exhaustion). • Infection, sepsis. • Burns (probably due to resetting of central thermostat). • Acute hepatic failure. • Mismatched blood transfusion (release of pyrogens). • Endocrine disorders (e.g. hyperthyroidism, phaeochromocytoma). • CNS disorders (e.g. head injury, SAH, meningitis, encephalitis, seizures). • Toxicity (e.g. amphetamines, including ecstasy, salicylates, cocaine, phencyclidine, lysergic acid diethylamide/LSD). A number of factors can predispose to developing hyperthermia: • Dehydration, hyperactivity/overexertion. • Illnesses: Parkinsonism, delirium tremens, psychosis, cardiovascular disease, autonomic dysfunction, endocrine dysfunction. • Anticholinergics and phenothiazines (dsweating). • Salicylates (uncoupled oxidative phosphorylation). • Diuretics (dehydration). • Tricyclics/MAOI’s (muscle rigidity, dsweating). • α/β-blockers (dheat loss). • Sympathomimetics (i heat production, vasoconstriction). • Hallucinogenics (dsweating, i metabolism).

Presentation and assessment • Apathy, malaise, headache, dizziness, confusion, muscle rigidity/ dystonia, ataxia, focal neurological signs, syncope, seizures, coma. • Nausea and vomiting. • Tachycardia, arrhythmias, wide pulse pressure, hypotension. • Hyperventilation, exhaustion, hypercapnia, metabolic acidosis. Prolonged, untreated hyperthermia can lead to: • Cardiovascular failure, and/or ARDS. • Muscle damage/rhabdomyolysis; lactic acidosis; liver dysfunction. • DIC (denatured clotting factors; endothelial damage). • Renal failure (due to dehydration, hypotension, rhabdomyolysis). • Hypernatraemia, hypo/hyperkalaemia, hypocalcaemia.

Investigations • • • • •

ABGs (metabolic acidosis, hypercapnia). FBC (iWCC/platelets in NMS, dplatelets in DIC). Coagulation screen (iPT/APTT, dfibrinogen in DIC). U&Es (hyperkalaemia, raised urea/creatinine), LFTs (may be deranged). Serum phosphate (i), serum calcium (d).

HYPERTHERMIA AND HEAT INJURY

• • • • •

CK (i in rhabdomyolysis), TFTs (exclude hyperthyroidism). Blood, urine and sputum cultures. Urine analysis (for toxicology and myoglobinuria). ECG (arrhythmias, if ACS suspected). CXR, CT scan or LP (if infection suspected).

Differential diagnoses • Specific syndromes causing hyperpyrexia (e.g. toxic epidermal necrolysis, NMS, MH, thyroid storm).

Immediate management • Give O2 and support airway, breathing, and circulation as required. • Give IV fluids, ideally guided by CVP and other invasive haemodynamic monitoring in cardiovascularly unstable patients. • Start cooling as soon as possible; options include: • Antipyretics (paracetamol and/or NSAIDs) • Peripheral cooling using exposure, tepid sponging, and fans • Cooling blankets and mattresses • Cold IV fluid infusions • Cold irrigation of: stomach, bladder, peritoneum, pleural spaces • Use of intravascular cooling systems (i.e. CoolGard™) • Haemofiltration using cold fluids • Sedation and ventilation along with neuromuscular block may be required to reduce heat production: • Hyperventilate to compensate for i CO2 production

Further management • Active cooling should continue until core temperature reaches 30% • Persistent organ failure

ACUTE SEVERE PANCREATITIS

Pancreatitis severity scoring Ranson criteria (score 1 for each of the following):1 • At presentation: • Age >55 • Blood glucose > 11 mmol/L 9 • White cell count >16 x 10 /L • Lactate dehydrogenase (LDH) >400 iu/L • AST >250 iu/L • Within 48 hours after presentation: • Haematocrit fall by >10% • Serum calcium 4 mmol/L • Blood urea rise >1 mmol/L • Fluid sequestration >6 L • PaO2 6 ~100% mortality Modified Glasgow scale (3 in 48 hours predicts severe disease)2 • Age >55. • PaO2 15 x 109/L. • Serum calcium 100iu/L. • Lactate dehydrogenase (LDH) >600 iu/L. • Blood glucose >10 mmol/L. • Serum albumin 16 mmol/L. Computed tomography grading A radiological grading system is also used ranging from A (normal) to D (the most severe grade, associated severe inflammation, necrosis or infection). 1

Reprinted with permission from the Journal of the American College of Surgeons, formerly Surgery Gynaecology & Obstetrics. ‘Prognostic signs and the role of operative management in acute pancreatitis’. Randon JHC, Rifkind KM, Roses DF, et al., Surg Gynecol Obstet 1974;139:69–81. 2 Reproduced from Gut, S.L. Blamey et al., ‘Prognostic factors in acute pancreatitis’, 25, 12, pp.1340–1346, copyright 1984, with permission from BMJ Publishing Group Ltd.

Further reading Balthazar et al. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002; 223(3): 603–13. Mier J, et al. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg 1997; 173: 71–5. Skipworth JRA, et al. Acute pancreatitis. Br J Intenisve Care 2010; 20(4): 105–15. UK Working Party on Acute Pancreatitis. UK guidelines for the management of acute pancreatitis. Gut 2005; 54(SIII): iii1–iii9. van Santvoort, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010; 362: 1491–502. Villatoro E, et al. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev 2010; 5: CD002941. DOI: 10.1002/14651858. CD002941.pub3. Whitcomb, D. Acute pancreatitis. N Engl J Med 2006; 354: 2142–50.

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Gastrointestinal and hepatic

2 The acute abdomen An acute abdomen (critical illness associated with marked abdominal signs, chiefly tenderness and rigidity) may be the cause of admission to ICU, or may occur whilst in critical care.

Causes • Generalized peritonitis due to perforated viscus (large bowel, small bowel, gastroduodenal ulcer): • Anastomotic breakdown should be suspected after surgery, especially if there was contamination and a p anastomosis • Traumatic perforation should be suspected where there is penetrating injury, or where there is blunt trauma causing major bruising or fractures of the spine, rib or pelvis • Infection from a bowel perforation or leak, or from another cause (e.g. spontaneous bacterial peritonitis, or in patients receiving CAPD). • Generalized peritonitis due to peritoneal irritation: • Haemorrhage (e.g. traumatic splenic rupture, ectopic pregnancy, a ruptured AAA, or surgical bleeding) • Bile leak (following biliary injury or after surgery) • Urine leak (following bladder trauma, or associated with surgery) • Localized peritonitis: diverticulitis, cholecystitis, appendicitis, abscesses.

Presentation and assessment Features associated with an acute abdomen include: • General: pyrexia; marked ‘third-space’ losses (e.g. oedema, ascites), with associated hypovolaemia; shoulder-tip pain. • Abdominal/GI: • Abdominal pain causing rigidity and prostration, with rebound and guarding (bowel obstruction may also cause colic) • Abdominal distension; absent, or altered, bowel sounds • Anorexia or lack of NG absorption, or large NG aspirates • Nausea and vomiting, diarrhoea, or bowel obstruction • An abdominal mass, or incarcerated hernias, may be present • If there has been recent surgery fluid may be present in wound drains (e.g. blood, faecal contents, urine) • Cardiovascular: hypotension, tachycardia (or occasionally a relative bradycardia); haemorrhage will result in associated signs ( b p.112). • Respiratory: tachypnoea/dyspnoea due to pain or metabolic acidosis. • Respiratory distress may occur due to abdominal splinting • Renal: oliguria (35 cmH2O)

ACS exists if IAP remains >20mmHg and new organ dysfunction occurs. 1 May be seen during mechanical ventilation, after surgery and in the obese. Reproduced with permission from the World Society of the Abdominal Compartment Syndrome.

Causes The risk factors for IAH include: • Trauma (especially blunt abdominal trauma, ACS develops in up to 15% of patients); pelvic fractures; massive transfusion. • Severe burns (especially with abdominal wall eschar formation). • Ascites or visceral oedema: infection, liver failure, pancreatitis, massive fluid resuscitation (>5 L in 24 hours); peritoneal dialysis. • Peritonitis, intra-abdominal abscesses. • Pneumoperitoneum, haemoperitoneum, haematoma. • Abdominal surgery (especially with p closure, ‘damage control’ laparotomy, incisional hernia repair, or retained surgical packs). • Bowel obstruction, ileus, volvulus. • Mechanical ventilation (especially with high levels of PEEP or prone positioning). • Obesity (BMI >30). • Tumour (abdominal or retroperitoneal). • Pneumonia, or sepsis from other causes. • Acidaemia (pH 30 degrees High body mass index (BMI), central obesity 2. Increased intra-luminal contents Gastroparesis Ileus Colonic pseudo-obstruction 3. Increased abdominal contents Hemoperitoneum / pneumoperitoneum Ascites / liver dysfunction 4. Capillary leak / fluid resuscitation

Acidosis (pH < 7.2) Hypotension Hypothermia (core temperature < 33°C) Polytransfusion (>10 units of blood / 24 hrs) Coagulopathy (platelets < 55000 / mm3 OR prothrombin time (PT) > 15 seconds OR partial thromboplastin time (PTT) > 2 times normal OR international standardised ratio (INR) > 1.5) Massive fluid resuscitation (>5 L / 24 hours) Pancreatitis Oliguria Sepsis Major trauma / burns Damage control laparotomy

IAH Grading Grade I Grade II Grade III Grade IV

Notify patient’s doctor of elevated IAP. Proceed to IAH / ACS management algorithm.

Observe patient. Recheck IAP if patient deteriorates clinically.

IAP 12–15 mmHg IAP 16–20 mmHg IAP 21–25 mmHg IAP >25 mmHg

Abbreviations IAH - intra-abdominal hypertension ACS - abdominal compartment syndrome IAP - intra-abdominal pressure

Fig. 8.1 Algorithm for assessment of intra-abdominal hypertension. Reproduced with permission from the World Society of the Abdominal Compartment Syndrome, 2006.

INTRA-ABDOMINAL HYPERTENSION

Intra-Abdominal Hypertension (IAH)

Patient has IAH (IAP > 12 mmHg)

NO

Initiate treatment to reduce IAP Avoid excessive fluid resuscitation Optimize organ perfusion

IAP > 20 mmHg with new organ failure?

NO

Monitor IAP with serial measurements at least every 4 hours while patient is critically ill

IAP < 12 mmHg consistently?

YES

YES

IAH has resolved Discontinue IAP measurements and monitor patient for clinical deterioration

Patient has ACS

Medical treatment options to reduce IAP 1. Improve abdominal wall compliance Sedation & analgesia Neuromuscular blockade Avoid head of bed > 30 degrees 2. Evacuate intra-luminal contents Nasogastric decompression Rectal decompression Gastro-/colo-prokinetic agents 3. Evacuate abdominal fluid collections Paracentesis Percutaneous drainage 4. Correct positive fluid balance Avoid excessive fluid resuscitation Diuretics Colloids hypertonic fluids Hemodialysis ultrafiltration 5. Organ Support Maintain APP  60 mmHg with vasopressors Optimize ventilation, alveolar recruitment Use transmural (tm) airway pressures Pplattm = Pplat – IAP Consider using volumetric preload indices If using PAOP/CVP, use transmural pressures PAOPtm = PAOP – 0.5 * IAP CVPtm = CVP – 0.5 * IAP

IDENTIFY AND TREAT UNDERLYING ETIOLOGY FOR PATIENT’S ACS

Definitions IAH - intra-abdominal hypertension ACS - abdominal compartment syndrome

Abdominal Compartment Syndrome (ACS)

Does patient have Primary ACS?

NO

IAP - intra-abdominal pressure

Patient has Secondary or Recurrent ACS

APP - abdominal perfusion pressure (MAP-IAP) Primary ACS - A condition associated with injury or disease in the abdomino-pelvic region that frequently requires early surgical or interventional radiological intervention

YES Perform / revise abdominal decompression with temporary abdominal closure as needed to reduce IAP

YES

Secondary ACS - ACS due to conditions that do not originate from the abdomino-pelvic region

Is IAP > 25 mmHg with progressive organ failure?

Recurrent ACS - The condition in which ACS redevelops following previous surgical or medical treatment of primary or secondary ACS

NO Continue medical treatment options to reduce IAP

Measure IAP/APP at least every 4 hours while patient is critically ill

NO

IAH has resolved Decrease frequency of IAP measurements and observe patient for deterioration

Perform balanced resuscitation of patient preload, contractility, and afterload using crystalloid / colloid / vasoactive medications AVOID EXCESSIVE FLUID RESUSCITATION

NO Can APP be maintained  60 mmHg?

YES

IAP < 12 mmHg consistently?

YES

Fig. 8.2 Algorithm for the management of intra-abdominal hypertension. Reproduced with permission from the World Society of the Abdominal Compartment Syndrome, 2006.

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Pitfalls/difficult situations • Open abdomen following decompression may lead to fluid loss (up to 20 L/day) and hypothermia; enteral feeding is often still possible. • If left untreated ACS leads to MOF with ~100% mortality.

Further reading Cheatham ML, et al. . Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med 2007; 33: 951–62. Malbrain MLNG, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006; 32(11): 1722–32. Maerz L, et al. Abdominal compartment syndrome. Crit Care Med 2008; 36(4s): s212–s215. World Society of the Abdominal Compartment Syndrome website: M

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3 Hepatic failure, hepatic encephalopathy, and hepatorenal syndrome Fulminant liver failure is defined as severe impairment of hepatic function or severe hepatocyte necrosis after liver injury in the absence of pre-existing liver disease. Hyper-acute liver failure exists if encephalopathy appears within 7 days of jaundice; acute liver failure if it appears within 8–28 days; and subacute if it appears between 29 days and 12 weeks. It is a syndrome rather than a disease, and so has a number of triggering aetiologies. Hepatorenal syndrome (HRS) is the development of renal failure in patients with severe liver disease in the absence of any other identifiable cause of renal pathology.

Causes • Drugs/toxins (e.g. paracetamol, the most common cause, sulphonamides, phenytoin, isoniazid, MAOIs, ecstasy, tetracycline, yellow phosphorus, Bacillus cereus toxin): • Idiosyncratic drug reactions (e.g. halothane, NSAIDs, rifampicin, valproic acid, disulfiram) • Infection (e.g. HAV, HBV, HCV, CMV, EBV, HSV, adenovirus, haemorrhagic fever viruses). • Toxins (e.g. Amanita phalloides mushrooms, carbon tetrachloride). • Alcohol. • Autoimmune hepatitis. • Malignancy (e.g. lymphoma, metastases). • Pregnancy related (e.g. acute fatty liver of pregnancy, HELLP syndrome). • Metabolic (e.g. Wilson’s disease, Reye’s syndrome, galactosaemia, hereditary fructose intolerance, tyrosinaemia). • Vascular (e.g. right heart failure, Budd–Chiari syndrome, veno-occlusive disease, ischaemic hepatitis). • Other (e.g. neurolept malignant syndrome, heat stroke, sepsis). Hepatorenal syndrome may: • Occur spontaneously in the setting of progressive liver failure. • Be associated with spontaneous bacterial peritonitis (SBP), sepsis, and large paracentesis without albumin replacement. • Arise from compensatory renal vasoconstriction secondary to systemic vasodilatation. Two types of hepatorenal syndrome exist: • Type 1; acute form: rapidly progressive renal failure occurs spontaneously in patients with severe liver disease (may be associated with SBP). • Type 2; chronic form: deterioration occurs over months, typically in patients with diuretic resistant ascites.

HEPATIC FAILURE

Presentation and assessment Hepatic failure may be associated with a history of viral illness, drug (paracetamol), or alcohol intake. Signs of chronic liver failure are not commonly present unless the present illness is ‘acute-on-chronic’: • General: jaundice. • Cardiovascular: vasodilatation, hyperdynamic circulation, lowered BP (predominantly diastolic) and tachycardia • i cardiac output and d SVR • Spikes of hypertension may indicate cerebral oedema • Respiratory: hypoxia due to i shunt fraction • Pulmonary aspiration, atelectasis, or chest infection • ARDS (up to 10% of patients) • Abdominal/GI: abdominal pain and retching (particularly with paracetamol poisoning) • Splenomegaly is typically absent in most cases, its presence may indicate Wilson’s disease or lymphoma • Renal: HRS may occur. Hepatic encephalopathy can be caused by acute fulminant hepatic failure, chronic liver failure decompensation, GI bleed, or trauma. • Grade 1: mild drowsiness, impaired cognition. • Grade 2: increasing drowsiness, confusion but conversant. • Grade 3: obeys simple commands but marked confusion. • Grade 4: responds only to painful stimuli, or not responsive. • Cerebral oedema is common with grade 3/4 hepatic encephalopathy. • Systemic hypertension, pupillary abnormalities, decerebrate posturing, hyperventilation, seizures and loss of brainstem reflexes may occur. Features associated with a worse prognosis in hepatic failure include: • Bleeding complications: GI bleeding is common; subconjuctival haemorrhage (in paracetamol poisoning); prolonged PT and low-grade DIC. • Metabolic complications: hypoglycaemia, hyponatraemia, hypokalaemia, hypophosphataemia, lactic acidosis. • Infections: pneumonia, UTI or sepsis.

Investigations • • • • • • • • • •

Group and save. ABGs (metabolic acidosis). FBC (raised WCC in infection, thrombocytopaenia in chronic disease). Coagulation screen (deranged clotting). U&Es. LFTs (albumin may be normal initially, AST and ALT may be >40 x normal initially but will fall with progression of damage). Serum glucose (hypoglycaemia occurs, monitor hourly). Serum magnesium, calcium, phosphate (hypophosphataemia and hypomagnesaemia are common); serum ammonia level. Drug screen (paracetamol). Viral serology (HAV-IgM, HbsAg; HBcore-IgM; EBV, CMV, HSV).

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• Blood, urine, sputum cultures (infections are common precipitants and are more common in patients with liver failure); ascitic fluid culture. • Urinary osmolality and electrolytes. • ECG (multiple VEs, heart block, bradycardia common). • CXR. • CT head (to exclude other causes of encephalopathy). • Abdominal US (metastases, lymphoma, venous patency, ascites). • Liver biopsy (rarely required). • Consider EEG (slow voltage waveforms in encephalopathy).

Hepatorenal syndrome The diagnosis of HRS requires the exclusion of other causes of renal failure in patients with liver disease. General signs and symptoms may include fatigue/malaise, systemic vasodilatation, hypotension, high cardiac output and evidence of liver failure/ ascites. The diagnostic criteria for HRS include: • Chronic or acute liver disease with advanced hepatic failure and portal hypertension. • Low GFR, as indicated by serum creatinine >225 μmol/L or creatinine clearance 6.5), irrespective of encephalopathy grade or 3 of: • PT >50s (INR >3.5) • Unfavourable aetiology (non-paracetamol, not Hep A or B) • Jaundice to encephalopathy >7 days • Age 40 years • Bilirubin >300 μmol/L (>17.6 mg/dl). With kind permisssion from Springer Science+Business Media, Current Treatment Options in Gastroenterology, ‘Fulminant Hepatic Failure’, 6, 6, 2003, pp.473–479, Albert J. Chang.

Pitfalls/difficult situations • Early referral to specialist centre is important. • Volume status can be difficult to assess. • The presence of ARDS, renal failure, and grade 4 encephalopathy are associated with worse prognosis. • The cause of the hepatic failure may not be clear, or hepatic failure may be due to ‘acute on chronic’ disease. • Distribution and metabolism of the drugs will be altered, consult hepatologists and pharmacists on dose adjustments. • Severe fluctuations in blood glucose are common; hypoglycaemia is a consequence of i circulating insulin, impaired gluconeogenesis and an inability to mobilize liver glycogen. • Respiratory alkalosis due to hyperventilation may occur; may be exacerbated by metabolic alkalosis due to hypokalaemia, or continuous gastric aspiration.

HEPATIC FAILURE

• In patients with fulminant hepatic failure or decompensated chronic liver disease, the presence of a metabolic acidosis that does not respond to volume loading is associated with a very poor outlook. • Encephalopathy may be very difficult to in intubated patients; acute confusional state may have been obvious pre-intubation (stage 1), but deep coma despite cessation of sedation may indicate stage 4. • Cerebral oedema requires high index of suspicion to detect (irreversible brain injury is associated with ICP >30 mmHg, or CPP 1000 ml or >20% estimated blood volume) is predicted in a critically ill patient (e.g. a patient with critical illness who has to undergo a major surgical procedure) consider: • Administering antifibrinolytics: tranexamic acid IV (loading dose 1g); protamine is no longer recommended. • Perioperative cell salvage.

BLOOD PRODUCT TRANSFUSION AND TRANSFUSION REACTIONS

Haemoglobin transfusion triggers A conservative blood transfusion policy should be used within critical care. The transfusion trigger should be • Ongoing bleeding/early septic shock: 8–10 g/dl • Known ischaemic heart disease: 10 g/dl • Symptomatic anaemia (e.g. dyspnoeic): 9–10 g/dl • All other cases: 7–9 g/dl • It is also suggested that patients with burns, cerebrovascular disease or head injury should share a transfusion trigger of 8–10 g/dl

Safety requirements Transfusion of blood products requires a ‘zero-tolerance’ approach to sampling, prescribing, and administration (Fig. 9.1), and should include: • Crossmatch samples should be taken from one patient at a time: • Patients should be identified by full name, date of birth and hospital/NHS number (by wrist band and verbally if possible) • Sample tubes should be hand-written at the bedside • All products should be prescribed using a record which contains full patient identification as just described. • Administration of blood products should only occur after a 2-person check of blood products, prescription and patient identification: • Any errors should prompt the administration to be abandoned • Details of the transfusion, including start/finish times and serial numbers should be recorded There is a legal requirement to keep a traceable record of all blood products transfused in Europe.

Special measures This refers to the need for irradiated or CMV negative blood products. In the following cases transfusion should be discussed with a haematologist in case special measures are required: • Patients who have had, or who may require, haematopoietic stem cell transplants (‘bone marrow transplants’). • Patients with Hodgkin’s disease, ALL, or aplastic anaemia. • After purine analogues (e.g. fludarabine), or pentostatin. • Patients with CLL treated with Campath 1H (alemtuzumab).

Patient refusal Adult patients, in particular Jehovah’s Witness patients, have an absolute right to refuse blood product transfusions. This may differ from patient to patient and some techniques, such as cell salvage, may be acceptable to some. This should be discussed in detail with them.

Complications • Acute transfusion reaction: • Hypotension, fever, or allergic reactions occurring within 24 hours of a transfusion

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• Error in transfusion requirements or administration; inappropriate/ unnecessary transfusion: • Failure to adhere to ‘cold chain’, or excessive administration time (>3.5 hours) • Use of expired red cells • Failure to administer anti-D • Failure to apply special measures (irradiated/CMV negative products) • Over-transfusion as a result of blood sample laboratory errors or over-enthusiastic transfusion prescribing • Haemolytic transfusion reaction: • Most commonly occurs if ABO incompatible blood transfused, but can involve uncommon antibodies, or bacterial overgrowth • Associated with fever/rigors, chest, back or abdominal pain, sweating, tachycardia and hypotension, tachypnoea and cyanosis, oliguria, haemoglobinuria, DIC • Can be acute or delayed in onset • More common in patients with sickle cell disease • Transfusion associated circulatory overload (TACO): • Within 6 hours of a transfusion, any 4 of: tachypnoea/dyspnoea, tachycardia, hypertension, pulmonary oedema, peripheral oedema • Transfusion-related acute lung injury (TRALI): • Occurs within 6 hours of plasma administration (FFP and platelets), resulting in hypoxia, hypotension, fever, and CXR findings consistent with pulmonary oedema (with a normal/low CVP) • Transfusion associated dyspnoea (TAD): • New respiratory distress within 24 hours of transfusion which is not TACO or TRALI • Transfusion-associated graft-versus-host disease: • Fever, rash, liver dysfunction, diarrhoea, pancytopaenia and marrow hypoplasia 100 ml/hr • Give furosemide if urine output falls/absent • Treat any DIC with appropriate blood components • Inform hospital transfusion department immediately

Mild fever

Reaction involves mild fever or urticarial rash only

No Severe allergic reaction

Yes

Suspected ABO incompatibility

No

Severe allergic reaction Haemolytic reaction/bacterial infection of unit • Stop transfusion • Take down unit and giving set • Return intact to blood bank along with all other used/unused units • Take blood cultures, repeat blood group/crossmatch/FBC, coagulation screen, biochemistry, urinalysis • Monitor urine output • Commence broad spectrum antibiotics if suspected bacterial infection • Commence oxygen and fluid support • Seek haematological and intensive care advice Fluid overload • Give oxygen and furosemide 40–80 mg iv

Mild allergic reaction Urticaria • Give chlorphenamine 10 mg slowly iv and restart the transfusion at a slower rate and observe more frequently

Yes

No

Yes

Bronchospasm, angioedema, abdominal pain, hypotension • Stop transfusion • Take down unit and giving set • Return intact to blood bank along with all other used/unused units • Give chlopheniramine 10 mg slow iv • Commence O2 • Give salbutamol nebuliser • If severe hypotension, give adrenaline (0.5 ml of 1 in 1000 intramuscular)* • Clotted sample to transfusion laboratory • Saline wash future components (* equivalent to 0.5 mg im)

Other haemaolytic reaction/bacterial contamination

No

Raised CVP

Acute dyspnoea/ hypotension Monitor blood gases Perform CXR Measure CVP/ pulmonary capillary pressure

Normal CVP

TRALI • Clinical features of acute LVF with fever and chills • Discontinue transfusion • Give 100% oxygen • Treat as ARDS – ventilate if hypoxia indicates

Fig. 9.1 Management of acute transfusion reactions. Reproduced from the Handbook of transfusion medicine, 4th edn, United Kingdom Blood Services, 2007.

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3 Clotting derangement Abnormally delayed blood clotting may occur due to deficiencies in amount and/or function of coagulation factors and platelets. Clinically, this may lead to problems with bleeding, purpura, and bruising. In the critically ill, deranged haemostasis is often multifactorial.

Causes Acquired coagulation factor deficiency • Dilution s to massive transfusion. • Liver failure. • Consumption (e.g. DIC, extracorporeal circulation). • Drugs (e.g. heparin, warfarin). • Nutritional deficiency, particularly vitamin K. • Autoantibodies (e.g. lupus anticoagulant, anti-Factor VIII antibody). • Primary fibrinolysis (e.g. burns, neurosurgery, malignancy). • Amyloid (Factor X deficiency). Inherited coagulation factor deficiency • Haemophilia A (Factor VIII deficiency) and B (Factor IX deficiency, Christmas disease). • von Willebrand’s disease (Factor VIII deficiency/platelet dysfunction). Thrombocytopaenia, caused by reduced platelet production • Marrow infiltration by malignancy. • Marrow failure (e.g. critical illness, sepsis, viruses). • Nutritional deficiency (e.g. vitamin B12, folate). • Drugs (e.g. cytotoxics, alcohol). Thrombocytopaenia, caused by i platelet consumption • DIC (see b p.306). • HUS/TTP. • Immune destruction (e.g. heparin-induced thrombocytopaenia (HIT, see b p.305), idiopathic thrombocytopaenic purpura, HIV, SLE). • Drugs (e.g. penicillins, anticonvulsants, antituberculous drugs). • Hypersplenism. • Extracorporeal circuits. Platelet dysfunction • Drugs (e.g. aspirin, NSAIDs, clopidogrel, abciximab). • Uraemia. • Liver failure. • Leukaemias. • Inherited platelet disorders (rare), e.g. Glanzmann’s disease, Bernard– Soulier syndrome.

Presentation and assessment • Haemorrhage, including intraoperative failure to achieve haemostasis. • Oozing from wounds and drain sites. • Spontaneous bleeding, bruising, or purpura (atypical sites such as muscles and joints may be involved). • Incidental finding on haematological investigation.

CLOTTING DERANGEMENT

Investigations Basic investigations should include: • G&S. • FBC (includes platelets). • Coagulation screen (PT, APTT and TT) and fibrinogen. • U&Es, LFTs. Involvement of a haematologist is required in many cases as more specialized haematological tests may be indicated, for example: • Blood film and/or bone marrow aspirate. • Antiplatelet antibody tests/autoantibody screen. • Platelet function tests. • Specific coagulation factor levels. • FDPs, D-dimers.

Differential diagnoses • • • •

Meningococcal, streptococcal septicaemia; infective embolic rashes. Ongoing bleeding. Over anticoagulation. Lab error, or sample contamination (i.e. from IV drip arm).

Immediate management Give O2 as required, support airway, breathing, and circulation. • If the patient is clinically shocked, begin fluid resuscitation, following a major haemorrhage protocol if appropriate (see b p.115) • Maintain a high index of suspicion for ‘surgical’ or other bleeding and stop local bleeding where possible: • In postoperative patients or following trauma • Following invasive procedures and line insertion • In patients at risk of GI bleeding • Send urgent blood for crossmatch, FBC and coagulation screen • Avoid hypothermia and acidosis (both impair coagulation) • Avoid/stop NSAIDS, anticoagulants; avoid IM injections • In cases of major trauma or major haemorrhage 1 g IV tranexamic acid may decrease the amount of blood loss due to fibrinolysis.

Coagulopathy • 10–15 ml/kg1 FFP, will rapidly reverse of clotting factor deficiency: aim for an INR 100 x 109/L • In chronic thrombocytopaenia without bleeding aim for a platelet count >10 x 109/L • 1 adult dose2 will raise the platelet count by 710 x 109/L • ‘Antiplatelet’ drugs should be stopped; irreversible drugs such as clopidogrel or aspirin mean that transfusion may be necessary despite apparently normal platelet numbers 1 2

1 bag of FFP is ~300 ml. 1 adult dose of platelets = 5 units.

Further management • Ongoing transfusion necessitates regular coagulation studies and platelet counts, as does critical illness. • Ongoing bleeding in the face of normal coagulation studies and platelet numbers should prompt a thorough search for a surgical cause. • Avoid hypothermia, acidosis, and correct hypocalcaemia (calcium is an important cofactor in the coagulation cascade). • Thrombocytopaenia/platelet dysfunction: • Involvement of a haematologist is indicated if no cause is apparent as bone marrow biopsy or specialist tests to diagnose and quantify abnormal platelet function may be required • Immune thrombocytopaenia (ITP) is treated with IV immunoglobulin and steroids; platelets are rarely indicated • Thrombotic thrombocytopaenic purpura/haemolytic uraemic syndrome (HUS/TTP) requires specialist haematology/renal input; platelet transfusions may result in further thromboses • Dialysis and desmopressin can be used in the setting of platelet dysfunction s to uraemia

Pitfalls/difficult situations • Irreversible ‘antiplatelet’ drugs, particularly aspirin and clopidogrel, should be stopped 5–10 days before surgery and invasive procedures. • FFP and cryoprecipitate take up to 30 minutes to thaw. • Platelets are held centrally and may time to reach peripheral hospitals. • Be careful with NGT or urinary catheter insertion in the coagulopathic. • In coagulopathic patients minor trauma can cause catastrophic bleeds.

Further reading Balikai G, et al. Haemotological problems in intensivse care. Anaesthes Intensive Care Med 2009; 10(4): 176–8. DeLoughery TG. Thrombocytopaenia in critical care patients. J Intensive Care Med 2002; 17(6): 267–82. George JN. Evaluation and management of pateints with thrombotic thrombocytopenic purpura. J Intens Care Med 2007; 22(82): 82–91. Keeling D et al. The management of heparin induced thrombocytopaenia. Br J Haematol 2006; 133: 259–69.

CLOTTING DERANGEMENT

Clotting function tests • Prothrombin time (PT; normal 12–14 seconds): • Assesses factor VII activity (extrinsic coagulation pathway) • Prolonged in liver disease, warfarin, vitamin K deficiency • Activated partial thromboplastin time (APTT; normal 25–35 seconds): • Assesses factors VIII, IX, XI, XII (intrinsic coagulation pathway) • Normal PT and prolonged APTT suggests heparin use, or inherited defect (von Willebrand’s disease, antiphospholipid syndrome, haemophilia) • Prolonged APTT and PT: liver disease, DIC, warfarin • Thrombin time (TT; normal 10–12 seconds): • Assesses thrombin and fibrinogen (common clotting pathway) • Prolonged with heparin, fibrinogen defect, FDPs • Prolonged APTT, PT, and TT: heparin, defective fibrinogen • Platelet count (thrombocytopaenia is a count 50%, or nadir 20–100 x 10 /L 9 • 1 point: fall in platelet count of 30–50%, or nadir 10–19 x 10 /L 9 • 0 points: fall in platelet count of 6 seconds; 1 point: 3–6 seconds; 0 points: 2 standard deviations). • Arterial hypotension (MAP 60 seconds or platelet count 70 μmol/L. • Lactate >1.6 mmol/L. • Mottling or i capillary refill time. Septic shock Sepsis with associated hypotension, or hypoperfusion (e.g. oliguria) after adequate fluid resuscitation. Severe sepsis • Sepsis with evidence of organ dysfunction: • ALI with PaO2/FiO2 ratio 34 μmol/L. 1

SIRS is the response to a variety of clinical insults resulting in with t2 of the first 4 signs.

Causes Causes of SIRS include: infection, trauma or burns, pancreatitis, infarction: myocardial, intracerebral, bowel, pulmonary embolism, drug and alcohol withdrawal, massive blood transfusion.

SEPSIS

Infections causing sepsis may be community or hospital/health-care acquired (ICU acquired is a subset). Common sites of infection include: • Respiratory (738%). • Device related (75%). • Wound/soft tissue (79%). • Genitourinary (79%). • Abdominal (79%). • Endocarditis (71.5%). • CNS (71.5%). The natural defences against infection may be disrupted by: • Trauma, burns, or major surgery (especially GI, GU surgery, or debridement of localized infections). • Intestinal obstruction/distension; gut ischaemia or perforation. • Endotracheal intubation or tracheostomy. • Indwelling intravascular catheters, urinary catheters and wound drains. • Intravenous infusions of fluids, drugs and nutrition. In immunocompromised patients unusual, multiple or opportunistic infections (e.g. fungal) may be seen. Common causes of immunocompromise include: • Drug treatment: chemotherapy, steroids. • Haematopoietic stem cell transplants. • Radiation injury. • AIDS. • Malnutrition, alcohol/drug abuse, or prolonged systemic disorders (including renal failure, hepatic failure, malignancy, multiple infections). • Multiple trauma, major surgery, multiple blood transfusions.

Presentation and assessment Presentation of infections, SIRS and sepsis varies according to infection site/type, and comorbidities. Non-localizing signs/symptoms include: • General: pyrexia (or hypothermia, particularly in the elderly or immunocompromised), sweats, rigors. • Respiratory: tachypnoea and hypoxia. • Cardiovascular: tachycardia (bradycardia may be a pre-terminal sign): • Peripheral vasodilatation (warm peripheries); or peripheral shut-down (cold peripheries) usually as late manifestation • icardiac output if monitored, (though it may decrease in severe sepsis) and d systemic vascular resistance • Poor perfusion (metabolic acidosis, raised lactate) • Hypertension or hypotension/shock • d JVP, CVP, or PAOP • Arrhythmias, particularly AF, atrial flutter or VT • Angina, or evidence of cardiac ischaemia • Peripheral/dependent oedema • Neurological: agitation, confusion, diminished consciousness, syncope. • Renal: oliguria, raised urea and creatinine. • GI: anorexia, nausea and vomiting. • Haematology: raised or lowered WCC; DIC. • Other: raised inflammatory markers (CRP, ESR, PCT). • Multiorgan dysfunction syndrome, or failure (MODS or MOF).

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Investigations • ABGs (metabolic acidosis, hypoxia). • FBC (raised/lowered WCC, thrombocytopaenia/thrombocytosis). • Coagulation screen, including D-dimers and fibrinogen (DIC, D-dimers may also be raised in response to inflammation). • U&Es, LFTs (renal/hepatic dysfunction, hyponatraemia). • Serum calcium, magnesium, phosphate. • Serum glucose (hypo/hyperglycaemia). • ECG. Some investigations may also confirm the likelihood of sepsis, or identify the source or type of organisms involved: • CRP (and to a lesser extent ESR; CRP is raised in inflammation, particularly so with infection). • Serum procalcitonin (PCT; used in some centres to help differentiate inflammation from infection). • Serum (and urine) antigen or antibody tests may be available for some organisms, including: • Legionella and Pneumococcal antigens are routinely tested in urine • Mycoplasma • Many viruses (HIV, HTLV, hepatitis A/B/C/D/E, EBV, CMV) • Protozoal or helminthic infections • Bacteriology, 1 or more of the following samples: 1 • Septic screen: blood, urine, and sputum cultures • Wound swabs; drain fluid (wound, chest, or other drains) • Nose and throat swabs (for culture and/or viral PCR) • Stool (for culture or for toxin detection, e.g. C. difficile toxin) • CSF (LP may also reveal other findings, b p.574) • If any invasive lines are removed, line-tips may be sent for culture • Some institutions take brush samples from CVCs • BAL samples (samples may be sent for bacterial, fungal, specialist culture or tests, e.g. AFBs for TB; viral PCR; immunofluorescence, galactomannan) • Samples of ‘tapped’ fluid (e.g. ascites, pleural fluid) • Speculum exam and vaginal swabs • Gram stains may be useful where rapid identification of any organism is significant (e.g. in CSF), or where unusual organisms are significant (e.g. gut organisms in pleural fluid); in other situations they do not aid diagnosis (e.g. Gram stain of BAL samples). • CXR (pneumonia, mediastinitis, perforated viscus). • US and/or CT scan of chest, abdomen (including renal and hepatic), head, or pelvis for evidence of a collection. • Echocardiography (TTE or TOE) for suspected endocarditis or to assess any LV dysfunction.

Differential diagnoses • Any non-infectious disease which causes an inflammatory response. • Infection from another site. 1 Blood cultures should be taken from every invasive line, as well as 1–2 percutaneous venous samples; percutaneous venous stabs should be taken from different sites to minimize the risk of skin contamination.

SEPSIS

Immediate management • Give O2, titrate to SaO2 of 94–98%. Airway: endotracheal intubation may be required. • Where infection or threatens airway patency. • Where there is dconsciousness (GCS d8). • To facilitate mechanical ventilation. Breathing: ensure breathing/ventilation is adequate. • Fatigue may lead to respiratory failure; CPAP and/or non-invasive BIPAP may be indicated. • Mechanical ventilation may optimize oxygenation in severe shock. • Respiratory infections may compromise breathing and require mechanical ventilation. Circulation: support should be commenced in patients with hypotension or elevated serum lactate. • Large peripheral venous cannulae are required. • Arterial and/or central venous cannulation should be undertaken as soon as feasible, checking coagulation studies and platelets first. • Resuscitate with crystalloids/colloids, (in first 6 hours), aiming for: • MAP t65 mmHg • CVP 8–12 mmHg (12–15 mmHg if mechanically ventilated) • Urine output t0.5 ml/kg/hour • CVC oxygen saturations t70% (or mixed venous >65%) • If venous SaO2 not achieved consider: • Further fluid resuscitation or dobutamine up to 20 mcg/kg/minute • Packed red cells transfusion if Hb < 7g/dl, (10g/dl if there is cardiac ischaemia or ongoing haemorrhage); or to achieve a haematocrit of t30% if venous oxygen saturation 70 years, ARDS, leucopaenia, hypothermia, DIC, multiple-organ (>2) failure.

Further reading Albert M, et al. Utility of Gram stain in the clinical management of suspected ventilator-associated pneumonia. Secondary analysis of a multicenter randomized trial. J Crit Care 2008; 23: 74–81. Dellinger RP, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock. Intensive Care Med 2008; 34: 17–61. Harrison DA, et al. The epidemiology of severe sepsis in England, Wales and Northern Ireland, 1996 to 2004: secondary analysis of a high quality clinical database, the ICNARC Case Mix Programme Database. Crit Care 2006; 10:R42 (doi:10.1186/cc4854). Kumar A, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006; 34(6): 1589–96. Kwok ESH, et al. Use of methylene blue in sepsis: a systematic review. J Intensive Care Med 2006; 21:359–63. Otero RM, et al. Early goal-directed therapy in severe sepsis and septic shock revisited: concepts, controversies, and contemporary findings. Chest 2006; 130: 1579–95. Rivers E, et al. Early goal directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345:1368–77. Russell JA, et al. Vasopressin versus norepinephrine in patients with septic shock. N Engl J Med 2008; 358(9): 877–87. Sprung CL, et al. Hydrocortisone therapy for patients with septic shock (CORTICUS). N Engl J Med 2008; 358: 111–24.

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2 Fever Within intensive care a core body temperature t38.3°C is considered a significant fever.

Causes Within ICU the commonest cause of pyrexia is infection: • Intravascular devices and implants. • Pneumonia, VAP. • Intra-abdominal collections. • Colitis (especially C. difficile). • UTI, urinary catheter related sepsis. • Sinusitis (especially if using nasogastric or naso-endotracheal tubes). • Surgical site infections. • ‘Occult’, unusual, or difficult to culture infections (e.g. infective endocarditis (IE), CNS infections, viruses (including CMV, fungal, TB). Non-infectious causes: • Postoperative fever. • Drug fever (e.g. β-lactam related), or drug withdrawal (e.g. alcohol). • Malignancy: lymphoma, leukaemia, solid cell tumours (especially renal), tumour lysis syndrome. • Connective tissue diseases: SLE, RA, PMR, sarcoid, vasculitis. • Infarction: myocardial, intracerebral, bowel, PE, fat emboli, stroke. • Venous thrombosis. • Inflammation: SIRS, ARDS, cytokine storm, hepatitis, pancreatitis, burns, gout, Dressler syndrome, immune reconstitution syndrome, Jarisch–Herxheimer reaction, transplant rejection. • Endocrine/metabolic: adrenal insufficiency, thyroid storm, malignant hyperpyrexia, NMS. • Blood product transfusion.

Presentation and assessment Pyrexia may be associated with other evidence of infection, including: • Tachypnoea, tachycardia, rigors, sweats. • Complications of sepsis (see b p.322). • Raised WCC and/or inflammatory markers. Other signs and symptoms may help identify the cause of the infection:1 • Altered mentation: meningitis (TB, cryptococcal, carcinomatous, sarcoid), brucellosis, typhoid fever. • Arthritis/arthralgia: SLE, infective endocarditis, Lyme disease, lymphogranuloma venereum, Whipple’s disease, brucellosis, inflammatory bowel disease. • Animal contact: brucellosis, toxoplasmosis, cat scratch disease, psittacosis, leptospirosis, Q fever, rat bite fever. • Cough: tuberculosis, Q fever, typhoid fever, sarcoidosis, Legionella. • Epistaxis: Wegener’s granulomatosis, relapsing fever, psittacosis. • Epididymo-orchitis: TB, lymphoma, polyarteritis nodosa, brucellosis, leptospirosis, infectious mononucleosis.

FEVER

• Hepatomegaly: lymphoma, disseminated TB, metastatic carcinoma of liver, alcoholic liver disease, hepatoma, relapsing fever, granulomatous hepatitis, Q fever, typhoid fever, malaria, visceral leishmaniasis. • Lymphadenopathy: lymphoma, cat scratch disease, TB, lymphomogranuloma venereum, infectious mononucleosis, CMV infection, toxoplasmosis, HIV, brucellosis, Whipple’s disease, Kikuchi’s disease. • Renal angle tenderness: perinephric abscess, chronic pyelonephritis. • Splenomegaly: leukaemia, lymphoma, TB, brucellosis, subacute bacterial endocarditis, cytomegalovirus infection, EBV mononucleosis, rheumatoid arthritis, sarcoidosis, psittacosis, relapsing fever, alcoholic liver disease, typhoid fever, Kikuchi’s disease. • Splenic abscess: subacute bacterial endocarditis, brucellosis, enteric fever, melioidosis. • Conjunctival suffusion: leptospirosis, relapsing fever, Rocky Mountain spotted fever. • Subconjunctival haemorrhage: infective endocarditis, trichinosis, leptospirosis. • Uveitis: TB, sarcoidosis, adult Still’s disease, systemic lupus erythematosus, Behçet’s disease.

Investigations • • • • •

• • • • •

FBC and differential (check for eosinophils). CRP, ESR. U&Es, LFTs, serum amylase, TFTs. Blood culture from all lines, and a peripheral ‘stab’. Samples for culture with/without microscopy, Gram stain, fungal culture, AFBs: • Samples from all drains and any effusions that can be tapped • Sputum; ideally BAL or protected specimen if intubated (for culture, immunofluorescence, PCR) • Swabs from nose, throat, naso-pharynx and perineum (for culture and/or viral PCR) • Urine (also do a dipstick test) • Serum for HIV (and possibly also toxoplasmosis, brucellosis, coxiellosis, EBV, CMV) • If diarrhoea is present stool culture and C. difficile toxin testing • If neurological symptoms present CT and/or LP • Blood smear if malaria a possibility ECG. CXR. Consider TTE or TOE if endocarditis is suspected. Other imaging: US of abdomen, CT of any suspect area (especially after major surgery), sinus X-rays, white cell scans. Consider autoantibody screens (ANA, ANCA, RF); GI endoscopy; BM biopsy and culture, lymph node biopsy (if lymphadenopathy present); temporal artery biopsy.

Differential diagnoses • Exclude measurement errors (check core temperature if possible).

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Immediate management • Give O2 as required, support airway, breathing, and circulation • Review the patient’s history including, including drug history, sexual history, travel, occupation and exposure to animals. • Look for any obvious site of infection including: • Eyes, ears, mouth, PR/PV (exclude the presence of tampons) • Cannulae, epidural and catheter entry sites for redness/pus • Skin especially the back of the patient and buttocks • Check for enlarged lymph nodes • Review all previous investigations, looking for changes in inflammatory markers, WCC, i insulin requirements, alteration in oxygen requirements, i lactate, reduced absorption of feed • If the patient is unwell start empirical treatment with different broad spectrum antibiotics to those used previously, covering for HAIs (e.g. meropenem IV 500 mg 8-hourly and vancomycin IV 500 mg 6-hourly)

Further management • Remove as many non-essential invasive devices as possible, especially if blood drawn from a line produces a positive blood culture. • If blood cultures remain negative but the patient is still clinically unwell, continue broad-spectrum antibiotics for 48 hours and review. • Consider introducing antifungal medications if the patient condition is deteriorating and the fever remains high. • Treat with antipyrexial agents with/without surface cooling if there is limited cardiovascular reserve, brain injury, or pyrexia is >39.5°C.

Pitfalls/difficult situations • Pyrexia precedes other signs for t3 days in some infections, including viral hepatitis, EBV, measles, leptospirosis, typhoid. • TTE is often technically difficult on mechanically ventilated patients. • Hypothermia may also be associated with infection. • If temperature persists despite 5–7 days of adequate antibiotic cover stop antibiotics for 12 hours, re-culture, and start different antibiotics. • CVVH often causes low temperatures and can mask signs of fever. • Patients may become colonized, but not infected with, organisms. • Consider the possibility of rare/tropical infections; or biological agents. • Immunocompromised patients may be at risk from unusual infections which are difficult to identify/culture (see HIV, b p.376, and neutropaenia, b p.308); in neutropaenia micro-organisms may include:2 • Lung: Pseudomonas aeruginosa, Pneumococci, Alpha-haemolytic streptococci, Acinetobacter species, Klebsiella, Aspergilllus • Abdomen: E. coli, Pseudomonas aeruginosa, Clostridium spp., Enterococcus spp., Klebsiella spp. • Urogenital: E. coli, Klebsiella spp., Pseudomonas aeruginosa, • Soft tissue: S. aureus, Alpha-haemolytic streptococci • Intravascular catheters: coagulase negative staphylococci, Corynebacteriae, Propionibacterium species, Candida spp. • Unknown: coagulase negative staphylococci, E. coli, Enterococcus spp.

FEVER

Comprehensive history and physical examination

Potential diagnostic clues

Yes

Order appropriate and specific diagnostic tests

No Minimum obligatory investigations* CBC, electolytes, BUN/creatinine, ESR/CRP, CPK, LFT, urinalysis (with culture if pyuria is present), blood cultures x3, ANA, ANCA, RF, HIV antibody, PPD or interferon y release assay, CXR, abdominal ultrasound or CT with contrast

Potential diagnostic clues

Yes

Order appropriate diagnostic tests

No Cryoglobulin, chest/abdominal CT with contrast, temporal artery biopsy (in patients >55 years old), FDG-PET if ESR/CRP elevated (where available) or nuclear scintigraphy, echocardiography, bone marrow biopsy and culture after peripheral blood smear, toxoplasmosis/brucellosis/coxiellosis/EBV/CMV serology

Potential diagnostic clues

Yes

Order appropriate diagnostic tests

No Invasive tests (lymph node or liver biopsy, lumber puncture, etc) if indicated Watchful waiting and re-evaluation *Peripheral blood smear should be done at this stage if patient has recently travelled to malaria endemic areas or if CBC suggests bone marrow involvement. CBC=complete blood count; BUN=blood urea nitrogen; ESR=erythrocyte sedimentation rate; CRP=C-reactive protein; CPK=creatine phosphokinase; LFT=liver function test; ANA=antinuclear antibody; ANCA=antineutrophilic cytoplasmic antibody; RF=rheumatoid factor; PPD=purified protein dervative; CXR=chest radiograph; CT=computed tomography; FDG-PET=fluoro-2-deoxy-D-glucose-positron emission tomography, EBV=Epstein-Barr virus, CMV=cytomegalovirus.

Fig. 10.1 Algorithm for the evaluation of fever of unknown origin. Reproduced from British Medical Journal, Varghese GM, et al. Investigating and managing pyrexia of unknown origin in adults, 341: 878–81. Copyright 2010, with permission from BMJ Publishing Group Ltd.

References 1. Varghese GM, et al. Investigating and managing pyrexia of unknown origin in adults. Br Med J 2010; 341: 878–81. 2. Penack O, et al. Management of sepsis in neutropenic patients: guidelines of the infectious diseases: guidelines from the infectious diseases working party of the German Society of Hematology and Oncology. Ann Oncol 2011; 22(5): 1019–29.

Further reading Laupland KB. Fever in the critically ill medical patient. Crit Care Med 2009; 3(S): S273–S278. Marik PE. Fever in ICU. Chest 2000; 117: 855–69. O’Grady NP, et al. Guidelines for evaluation of new fever in critically ill adult patients: 2008 update from the American College of Critical Care Medicine and the Infectious Diseases Society of America. Crit Care Med 2008; 36: 1330–49.

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4 Airway infections and mediastinitis (See also b p.32.) Airway infections can cause localized inflammation and oedema with or without systemic sepsis. Infection may also spread into the deep tissues of the neck or mediastinum. Mediastinitis may also result from contiguous spread after oesophageal rupture or sternotomy.

Causes Airway infections • Pharyngeal, retropharyngeal, or peri-tonsillar abscess. • Ludwig’s angina or deep-neck infections (often polymicrobial). • Epiglottitis or diphtheria. Mediastinitis • Mediastinal extension of dental or neck infection. • Tracheal perforation. • Oesophageal perforation (traumatic, post-surgical anastomotic breakdown, spontaneous/Boerhaave syndrome); associated with malignancy or infection (e.g. TB). • Post-sternotomy surgical site infection (e.g. after cardiac surgery).

Presentation and assessment Signs/symptoms of infection ( b p.322) may be accompanied by: • Increasing respiratory distress, tachypnoea, dyspnoea, hypoxia. Airway infections may cause: • Stridor. • ‘Hunched’ posture; sitting forward, mouth open, tongue protruding. • ‘Muffled’ or hoarse voice, sore throat, painful swallowing, drooling . • Neck swelling, or trismus. Mediastinitis may be associated with: • A history of coughing, choking, or vomiting (Boerhaave syndrome). • Recent oesophageal surgery or endoscopy. • Signs associated with pneumothorax, or hydrothorax (i.e. percussion note and auscultation changes); most commonly left sided.

Investigations (See b p.324.) Other investigations will depend on the presentation, but may include: • Throat swabs.1 • Lateral soft tissue neck X-ray may demonstrate swelling and loss of airway cross-section (‘thumb print’ and ‘vallecula’ signs). • Laryngoscopy (indirect or fibreoptic).1 • CT or MRI of head and neck; or CT scan of chest. • CXR (pneumomediastinum, pneumothorax or hydrothorax). • Oesophagoscopy. • Water soluble contrast swallow (or barium swallow). 1 Airway interventions in a patient with a partially obstructed airway can provoke complete airway obstruction.

AIRWAY INFECTIONS AND MEDIASTINITIS

Differential diagnoses • Airway foreign body or tumour; traumatic pneumo- or haemothorax

Immediate management • Give O2 as required, support airway, breathing, and circulation. Airway infections • Airway intubation or tracheostomy is required in severe cases; anaesthetic and ENT input will be required (see b p.33) • Obtain IV access and consider steroids (dexamethasone 8 mg IV) Oesophageal perforation • Keep patient NBM • Insert intercostal chest drain(s) as indicated by X-ray findings Suggested empirical antimicrobials • Epiglottitis: cefotaxime 1–2 g IV 12-hourly • Deep-seated neck infections: clindamycin 600 mg IV 6-hourly, benzyl penicillin 600 mg IV 6-hourly, and metronidazole 500 mg IV 8-hourly • Diphtheria: clarithromycin 500 mg IV 12-hourly, and possibly anti-toxin (if strain is toxin producing) • Oesophageal perforation: piptazobactam IV 4.5 g 8-hourly and gentamicin IV 5 mg/kg daily and fluconazole IV 400 mg daily

Further management • Airway or dental abscesses should be assessed by ENT specialists in case surgical drainage or dental extraction is required. • Thoracic surgical advice should be sought where mediastinal collections or oesophageal perforation are suspected; early presentation of an oesophageal perforation may be amenable to repair. • Oesophageal perforation will require feeding to be post-pyloric (nasojejunal, or jejunostomy) or parenteral. • In cases of airway infection assess for airway swelling (laryngoscopy/ cuff-leak test) prior to extubation.

Pitfalls/difficult situations • In cases of airway infection, delaying intubation may make a difficult intubation impossible. • Spontaneous oesophageal rupture may present very late with gross contamination of the pleura and a large hydropneumothorax; small-bore chest drains are often insufficient.

Further reading Ames WA, et al. Adult epiglottitis: an under-recognized, life-threatening condition Br J Anaesth 2000; 85: 795–7. Ridder GJ, et al. Descending necrotizing mediastinitis: contemporary trends in etiology, diagnosis, management, and outcome. Ann Surg 2010; 251(3): 528–34. Kaman L, et al. Management of esophageal perforation in adults. Gastroenterol Res 2010; 3(6): 235–44. Khan AZ, et al. Boerhaave’s syndrome: diagnosis and surgical management. Surgeon 2007; 5(1): 39–44.

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3 Pneumonia and empyema (See also b p.62.) Pneumonia can occur as a result of infection acquired in the community or in hospital/health-care settings. In hospitalized patients, oropharyngeal overgrowth of enteric organisms, Pseudomonas, or Candida amongst the flora increases the risk of pneumonia after aspiration/micro-aspiration; pneumonia caused by drug-resistant organisms is also more common. Abscesses may occur within the lung, or infection may spread from the lung to a parapneumonic effusion, resulting in an empyema. The mortality from lung abscess or empyema is 10–20%.

Causes Pneumonia-causing organisms vary according to where it is acquired: • Community acquired pneumonia (CAP). • Hospital acquired pneumonia (HAP) or health-care associated pneumonia (HCAP). • Aspiration pneumonia or ventilator-acquired pneumonia (VAP). Infection may be caused by: • ‘Typical’ organisms (S. pneumoniae, H. influenzae). • ‘Atypical’ organisms (i.e. insensitive to penicillins: Legionella, Mycoplasma, Chlamydophila species, Coxiella burnetti). • Viruses (e.g. influenza A and B). • Uncommon organisms, often associated with chronic illness and hospitalization (S. aureus, M. catarrhalis, K. pneumonia, Pseudomonas, E. coli, Enterobacter, Acinetobacter). Where there is no response to treatment or the patient is immunocompromised consider less common causes: • ‘Unusual’ organisms: TB, Pneumocystis jiroveci, Stenotrophomonas, Cryptococcus neoformans. • Resistant species: MRSA, resistant Pseudomonas. • Viral: varicella, CMV. • Fungal: Candida spp., Aspergillus. Empyema: • Community-acquired empyema is most commonly associated with streptococcal infections (50%), as well as Staphylococci, anaerobes and Gram-negative organisms. • Hospital-acquired empyema is often caused by S. aureus (including MRSA), as well as Pseudomonas, E. coli, and Enterobacter. Lung abscess: • Organisms include aerobic organisms (S. aureus, H. influenzae, Klebsiella species, S. milleri, S. pyogenes) and anaerobes (Prevotella, Bacteroides, Fusobacterium spp.); often polymicrobial. • Associated with S. aureus, K. pneumonia, and Pseudomonas. • Associated with bronchial carcinoma, aspiration, prolonged pneumonia, liver disease, dental disease, and IV drug use (septic embolization). See Table 10.1 for incidence of pneumonia-causing organisms.

PNEUMONIA AND EMPYEMA

Presentation and assessment Signs and symptoms of infection ( b p.322) may be accompanied by: • Increasing respiratory distress, tachypnoea, dyspnoea. • Cough, purulent sputum, haemoptysis, or pleuritic chest pain. • Features of coexisting disease (e.g. COPD or bronchiectasis). • CXR changes of collapse, consolidation or parapneumonic effusion. Atypical pathogens should be suspected where the following are present: • Dry cough and/or multisystem involvement (e.g. headache, abnormal LFTs, elevated serum creatine kinase, hyponatraemia). • A history of travel, pets, high-risk occupations, comorbid disease. • Immunosuppressive disease or therapy. HAP, HCAP, VAP, or aspiration should be suspected in patients where: • Symptoms occur t48 hours after hospital admission. • The patient is readmitted d10 days after discharge from hospital. • Residence in a nursing home or extended care facility where there is recent or prolonged antibiotic use (e.g. leg ulcer treatment). • Receiving care for a chronic condition. • Patients with a neurological injury or d consciousness level. • Difficulty swallowing (e.g. stroke, Parkinson’s disease), or NG feeding. • In patients mechanically ventilated for >48 hours by means of an ETT or tracheostomy, where there is: • Worsening oxygenation or i sputum production • Indices of infection (pyrexia, WCC, CRP, culture results) • CXR changes on routine films Empyema: pleural effusion is a common ICU finding, suspect infection if: • Sepsis or inflammatory markers do not resolve. • Imaging suggests fibrin stranding or loculation. • Pleural tap reveals fluid that is turbid or has decreased pH. Multiple drug resistance (MDR) may be present if: • HAP/HCAP/VAP are suspected. • The patient has been on prolonged antibiotic therapy, or there is a failure to respond to appropriate antibiotics. • Immunosuppressive disease or therapy is present. • The patient is receiving care for a chronic condition (e.g. dialysis). • The patient, their relatives, or the place where they are treated, are known to be associated with multidrug-resistant pathogens.

Investigations (See b pp.63 and 324.) Also consider: • ABGs (hypoxia, acidosis, or respiratory alkalosis). • FBC (WCC may be high, >12, or low 2 L blood loss in 24 hours post-op. • Signs and symptoms of cardiac tamponade may rapidly appear (raised CVP/JVP, d cardiac output, hypotension, acidosis). • Clinical signs of hypovolaemic shock: hypotension, tachycardia,1 vasoconstriction/reduced pulse pressure, oliguria, thirst, agitation. • Development of organ failure is a late sign (e.g. reduced GCS).

Investigations • • • • • • • • • •

ABGs (metabolic acidosis, lactataemia suggest impaired perfusion). FBC (anaemia). Coagulation screen (i APTT/PT, d fibrinogen/platelets suggest DIC). TEG (if available offers rapid diagnosis of coagulation function). Crossmatch blood/blood products as appropriate. U&Es (hyperkalaemia following massive transfusion). Serum calcium (may be d following massive transfusion). CXR (haemothorax, pneumothorax). Transthoracic/transoesophageal ECHO (tamponade, MI, LVF) Chest US (haemothorax, pneumothorax).

Differential diagnoses • Cardiogenic shock (e.g. MI, PE, tension pneumothorax). • Hypovolaemic shock (haemorrhage from elsewhere, e.g. GI bleed). • Distributive shock (e.g. post-bypass SIRS).

Immediate management • Give O2 as required to maintain SpO2 t 95%, support airway and breathing (consider early endotracheal intubation). • Restore intravascular volume using crystalloids/colloids/blood; extra wide-bore peripheral access may be required. • Failure to respond/collapse/arrest are indications for chest reopening (see Fig. 11.1). • Consider protamine IV (1 mg/kg) for rebound heparinization.

1

Tachycardia may fail to develop in some patients.

HAEMORRHAGE AFTER CARDIAC SURGERY

Further management • Continue with respiratory support until cardiovascular stability is established; vasopressor support may be required initially. • Consider other haemostatic agents: tranexamic acid, aminocaproic acid (antifibrinolytics) or desmopressin (DDAVP).

Pitfalls/difficult situations • Platelet dysfunction may not be revealed by standard coagulation screen; TEG may aid management of coagulopathy. • Always involve haematology/blood bank for massive transfusions. • Adhere strictly to cross-checking procedures.

Further reading Dunning J, et al. Guideline for resuscitation in cardiac arrest after cardiac surgery. Eur J Cardiothorcic Surg 2009; 36(1): 3–28. Whitlock R, et al. Bleeding in cardiac surgery: Its prevention and treatment – an evidence-based review. Crit Care Clinics 2005; 21(3): 589–610.

CARDIAC ARREST assess rhythm ventricular fibrillation or tachycardia

asystole or severe bradycardia

DC shock (3 attempts)

pace (if wires available)

pulseless electrical activity

start basic life support amiodarone 300mg via central venous line

atropine 3mg consider external pacing

if paced, turn off pacing to exclude underlying VF

prepare for emergency resternotomy continue CPR with single DC shock every 2 minutes until resternotomy

continue CPR until resternotomy

continue CPR until resternotomy

airway and ventilation If ventilated turn FiO2 to 100% and switch off PEEP. change to bag/valve with 100% O2, verify ET tube position and cuff inflation and listen for breath sounds bilaterally to exclude a pneumothorax or haemothorax. If tension pneumothorax suspected, immediately place large bore cannula in the 2nd rib space anterior mid-clavicular line. DO NOT GIVE ADRENALINE unless a senior doctor advises this. If an IABP is in place change to pressure trigger. Do not delay basic life support for defibrillation or pacing for more than one minute.

Fig. 11.1 Resuscitation after cardiac surgery algorithm. Reproduced with permission from the European Journal of Cardiothoracic Surgery.

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Surgical patients

3 TUR syndrome TUR syndrome occurs when large volumes of hypotonic irrigating solution are absorbed rapidly into the circulation, resulting in rapid changes in serum osmolality and electrolyte concentrations. It most commonly occurs during transurethral resection of the prostate (TURP), but may be seen with bladder tumour resection (TURT), cystoscopy, lithotripsy, and transcervical endometrial resection (TCRE).

Causes • • • •

Prolonged surgery. High irrigation pressures. Extensive surgical field. Inadequate haemostasis.

Presentation and assessment Clinical features may include: • Confusion, agitation, headache. • Dyspnoea, tachypnoea, hypoxia. • Hypertension. • Nausea, vomiting. • Visual disturbance, blurred vision. Late signs include: • d level of consciousness, seizures. • Hypotension, arrhythmias, cardiac arrest.

Investigations • • • • • • •

ABGs (hypoxia, metabolic acidosis). FBC (anaemia). U&Es (hyponatraemia). Ammonia (i; major by-product of glycine metabolism). ECG (bradycardia, ST/T depression, wide QRS, SVT, VT). CXR (pulmonary oedema). Consider CT head if sodium normal.

Differential diagnoses Other causes of respiratory failure/shock: • Urosepsis (pyrexia, vasodilatory shock). • MI (NSTEMI/STEMI, LVF, cardiogenic shock). • PE (hypoxia, right heart strain, cardiogenic shock). • Haemorrhage (hypovolaemic shock).

Immediate management • Give O2 as required to maintain SpO2 t95%, support airway, breathing, and circulation. • Hypoxia or frank pulmonary oedema may require treatment with external CPAP/NIV or endotracheal intubation and mechanical ventilation. • Give furosemide IV 1 mg/kg (repeated doses may be required). • Consider mannitol 50–100 ml IV if the patient is symptomatic but does not have pulmonary oedema.

TUR SYNDROME

• Correct hyponatraemia: • Raising the serum sodium concentration by 1 mmol/L/hour may be taken as a safe rate + • Use saline 0.9% for gradual correction if Na >120 mmol/L + • Use hypertonic saline if Na 30 cm • Falls from height (>3 m, or 5 stairs); fall from a horse. • Sporting injuries. • Assaults. Penetrating mechanisms • Stabbings. • Gunshot wounds (GSWs). • Impalement. Any patient with a significant mechanism should be transported to a major trauma centre where a trauma team is on standby to receive them. Life-threatening injuries may have already been identified and managed in the p survey in the ED and operating theatre prior to the patient’s admission to critical care. However, new pathologies can develop, or old ones recur. Always return to the ATLS style of management should a trauma patient become unstable. Limb-threatening injuries (i.e. compartment syndrome) may not have been identified prior to ICU admission, or may have developed during resuscitative measures.

Life-threatening injuries • Airway obstruction (e.g. laryngeal or tracheal injury): • Head injury with impaired consciousness • Breathing injuries: • Pneumothorax (tension, open), or massive haemothorax • High spinal injury • Flail chest

TRAUMA

• Cardiac injuries (tamponade or cardiac contusion). • Severe haemorrhage: • Major arterial damage • Intra-abdominal bleeding • Pelvic fracture or bilateral femoral fractures • Acute coagulopathy of trauma • Intracranial lesions. • Hypothermia.

Limb-threatening injuries • • • • •

Traumatic amputation. Vascular injury/compromise. Open fracture. Compartment syndrome. Crush injury.

Approach Assessment of trauma patients should follow a set routine, elucidating and treating life- and limb-threatening injuries as they are found, in the order in which they will harm the patient (an ‘ATLS approach’). In all cases it is essential to ensure that those treating the patient are safe to carry out their work. A p survey (following the ABC format) should be performed and life-threatening injuries treated simultaneously. For example, if there is catastrophic haemorrhage (e.g. major blast/ballistic injury, or traumatic amputation) the p survey is be modified to deal with this first.

Trauma primary survey: ABC approach Primary survey • Airway (and C-spine or other spinal immobilization) • Breathing (and ventilatory control) • Circulation (and haemorrhage control) • Disability (and neurological care) • Exposure (and temperature control) Obtain a history and detailed information; the minimum should include an ‘AMPLE’ history (b p.2). Obtain information from the patient, relatives, or paramedics concerning the mechanism of injury Immediate investigations and decision-making • Bloods, including crossmatch and β-HCG as needed • CXR • Pelvic X-ray • Consider rapid US scan (focused assessment with sonography for trauma, ‘FAST’ scan) • Decision-making: is there a need for urgent transfer (e.g. for a CT scan, urgent surgery, transfer to a major trauma centre)?

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Trauma, burns, and skin injury

Immediate management • • • •

Give 100% O2, commence pulse oximetry, ECG, and BP monitoring. Commence C-spine/spinal control (Fig. 12.1). Perform p survey, initial resuscitation, and investigations. Obtain an AMPLE history (b p.2).

Primary survey Airway • Examine for: airway obstruction: d conscious level, foreign body/ matter, expanding neck haematoma, laryngeal fracture, stridor. • If obstruction is present perform a jaw thrust and insert an oro/ nasopharyngeal airway if required (chin lift and head-tilt should be avoided in patients with suspected C-spine injuries): • Avoid nasopharyngeal airways if BOS fracture is suspected • Where obstruction is present, or likely to occur, consider endotracheal intubation or an emergency needle cricothyroidotomy/ tracheostomy (see b pp.522 and 528). Breathing • Look for evidence of respiratory compromise: hypoxia (reduced PaO2 or SaO2), dyspnoea, and/or tachypnoea, absent or abnormal chest movement, loss of chest wall integrity (flail segment), pulmonary aspiration, massive bleeding. • Exclude/treat life-threatening conditions (e.g. tension pneumothorax, massive haemothorax1). • Consider endotracheal intubation and mechanical ventilation in patients with actual or imminent respiratory distress. Circulation • Look for evidence of circulatory inadequacy: tachycardia, weak pulse, hypotension, cold peripheries, prolonged capillary refill (>2 seconds, but difficult to interpret in associated hypothermia). • Look for obvious or concealed blood/fluid loss: palpate the abdomen, feel for blood pools (flanks, hollow of neck/back, groin), look for pelvic instability, look for long-bone fractures. • Exclude life-threatening conditions such as cardiac tamponade (raised CVP/JVP, pulsus paradoxus, diminished heart sounds, low voltage ECG), tension pneumothorax,2 haemorrhage or arrhythmia: • Assess degree of shock (b p.104) • Establish wide-bore IV access (2 x 16G cannulae), if not possible consider intraosseous or central access (b pp.536 and 542) • Commence fluid/blood replacement and treatment of hypovolaemic shock; give 500 ml of colloid within 5–10 minutes and reassess: • Follow a major haemorrhage protocol (b p.115) • Permissive hypotension (b p.106) may be appropriate in some cases whilst awaiting definitive haemorrhage control 1 The insertion of a chest drain to treat massive haemothorax may precipitate further catastrophic haemorrhage, obtain IV access first and have IV fluids prepared. 2 Tension pneumothorax may present as a respiratory or circulatory emergency.

TRAUMA

• Various initial resuscitation targets in trauma exist, one example is: • Head injury: systolic of 90 mmHg • Blunt trauma: systolic of 90 mmHg • Penetrating injury: systolic of 60–70 mmHg • Pre-existing hypertension: patient’s usual MAP • Haemorrhage control may require: • Direct pressure, or indirect pressure (e.g. femoral artery) • Elevation (where possible) • Wound packing • Windlass dressing, or tourniquets where required ® ® • Novel haemostatic agents (e.g. Celox , Quickclot ) Disability/neurology • Rapidly assess the patient’s neurological status using GCS or AVPU (Alert, responds to Voice, responds to Pain or is Unresponsive). • Check for pupil signs and plantar responses. • Check for Battle’s sign and scalp, nose, or ear haemorrhage; perform otoscopy now or during s survey. Exposure/general • Measure the patient’s core temperature: 3 • Rewarming should be commenced if required • Establish full exposure of affected area. • Provide analgesia as required. 3

Where ROSC has occurred following cardiac arrest, active warming may be inappropriate.

Investigations • ABGs may aid resuscitation. • Finger-prick blood sugar test should be measured. As soon as IV access is established take the following blood tests: • Crossmatch. • FBC (bedside Hb tests may be available). • Coagulation test (especially during haemorrhage resuscitation; bedside coagulation screen may be available). • U&Es, LFTs. • Serum glucose. • Consider paracetamol, salicylate, alcohol levels. • βHCG (in women of childbearing age). Also consider: • Bench co-oximetry for carbon monoxide. • ECG. • Where severe abdominal bleeding is suspected consider performing diagnostic peritoneal lavage (DPL) to confirm the presence of blood (where scanning is not available). Imaging of major trauma should include: • Lateral C-spine, CXR, pelvis X-ray. • Other long bones may be X-rayed as clinically indicated. • AP and ‘peg’ views of the C-spine may also be considered, but CT of neck may be more appropriate (see b pp.182 and 408).

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Obtunded patient with potential spinal injury. Full spinal immobilization CT head to exclude intracranial pathology

CT cervical spine C1 to T1 with 3D reconstruction Admitted to ITU with spinal immobilization

Formal radiologist’s report of CT imaging obtained

NORMAL

ABNORMAL

Remove spinal inmmobilization

Definitive managament or MRI

Fig. 12.1 Algorithm for ICU C-spine clearance. From Harrison P, et al. Clearing the cervical spine in the unconscious patient. Continuing Education in Anaesthesia, Critical Care and Pain 2008; 8: 117–20, by permission of Oxford University Press.

• CT of head, chest, neck, or abdomen/pelvis may be required. • Rapid US scanning may be available to detect haemorrhage; FAST scan can be used to rule in pericardial, hepato-renal, spleno-renal and pelvic haemorrhage. Other imaging that may be required: • Long-bone X-rays. • CT angiography. • Retrograde urethrogram.

Chest X-ray findings associated with traumatic aortic disruption • • • • • • • •

Widened mediastinum Distorted, poorly defined aortic knuckle Tracheal deviation (to the right) Loss of space between the pulmonary artery and the aorta Depression of the left main bronchus Oesophageal/nasogastric tube deviation (to the right) Paratracheal striping Left haemothorax

TRAUMA

• Fractures of ribs 1 or 2; scapula fractures • Pleural or apical caps • Widened paraspinal interfaces

Specific injuries involving critical care Spinal cord injuries • In major trauma all patients should initially be assumed to have a spinal injury and spinal precautions used including hard collar, sand bags, head strapping, and log-rolling: • The patient must be moved from the long board, once stable, onto a mattress to prevent early pressure sores developing • High spinal injuries (C1–C3) may present with dyspnoea, accessory muscle use, and ventilatory failure, necessitating early endotracheal intubation and ventilation: • Suxamethonium is safe to use within the first 48 hours of a spinal injury; once muscle atrophy occurs there is a risk of hyperkalaemia • Spinal shock and autonomic disruption may occur; other causes of hypotension such as occult haemorrhage should be excluded: • Spinal shock may require vasopressors • Bradycardia may occur • There is controversy about the use of high-dose steroids within the first 8 hours of spinal cord injuries: if used give methylprednisolone IV 30 mg/kg in 15 minutes, then 5.4 mg/kg/hour for 23 hours. • Where it has not been possible to rule out spinal cord injury in an unconscious patient admitted to the ICU, carry out the investigations recommended on b pp.182 and 408. • Thermoregulation: patients are unable to regulate body temperature and require warming in the early phase of the injury. • Urinary retention: all patients require catheterization. • Autonomic dysreflexia: sudden peripheral stimuli may precipitate hypertensive crises. • Considerations for the long-term care of paralysed patients may be found on b p.197. Airway damage (See b p.28.) Pneumothorax/tension pneumothorax (See b p.80.) • Open chest wounds have the potential to cause lung collapse and impaired gas exchange; sealing them completely risks development of a tension pneumothorax: • They should be sealed on 3 sides, with 1 side left free to allow air to escape; alternatively use Asherman or Bowlin chest seals. Haemothorax (See b p.82.) • This may occur early, at the time of the injury, or late if intercostal vessels are damaged by fractured ribs.

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Rib fractures, flail chest, pulmonary contusion • Severe pain may limit the ability of the patient to cough or deep breathe; a thoracic epidural may be required for pain relief: • Atelectasis and pneumonia may occur as a late complication of rib fractures, especially where respiration is limited by pain • The presence of rib fractures increases the likelihood of pneumothoraces, especially in mechanically ventilated patients. • The presence of multiple rib fractures, especially the upper 3–4 ribs, is associated with underlying lung, mediastinal, and C-spine injury. • Flail chest occurs when a segment of chest wall loses continuity with the rest of the bony structure (usually as a result of 2 fractures) and effectively ‘floats free’: • In normal respiration the chest can expand and generate a negative pressure, where a flail segment is present it may be sucked in by the negative pressure, rather than air through the airways • Paradoxical breathing may be obvious (flail segment moving in with respiration). • Dyspnoea, tachypnoea may be present. • Endotracheal intubation and mechanical ventilation are likely to be required. • Pulmonary contusions may develop in the first 24 hours after blunt chest injury causing characteristic CXR changes: • Lung injuries with associated rib, T-spine, or clavicular fractures are more likely to be affected • Increasing O2 requirement may indicate the need for endotracheal intubation and mechanical ventilation Cardiac tamponade (See b p.146.) Cardiac contusion • Cardiac contusion may occur as a result of blunt chest injuries. • Hypotension and ECG changes may occur: arrhythmias, VEs, sinus tachycardia, AF, RBBB, ST segment changes. • ECG monitoring should be continued for 24 hours as severe arrhythmias may develop. • Severe right-sided contusions may result in a raised CVP. • Myocardial ischaemia may have precipitated the trauma. • A troponin rise is common and does not usually represent ischaemic damage to the myocardium. • Contusion usually settles without significant cardiac comorbidity. Aortic disruption • Rapid deceleration injuries affecting the chest may cause disruption of the great vessels, which may initially be contained by haematoma. • Hypotension is normally caused by another bleeding site (as rapid aortic bleeding is mostly fatal). • The presence of CXR changes (see b p.408) should prompt CT angiography or TOE. • If suspected, obtain vascular or cardiothoracic surgical advice. • Avoid surges in BP; infusions of hypotensive agents such as labetalol or esmolol may be required.

TRAUMA

Shooting • ‘Low’-velocity (handgun bullets) injuries cause damage along the bullet track; ‘high’-velocity (rifle bullets) injuries may cause extensive cavitation areas within the wound. • Entrance/exit wound size does not predict the degree of wound cavity. • Bullet or bone fragments may cause further damage. • The wound tract will be soiled by environmental contaminants: • Wound exploration, debridement and excision may be undertaken; delayed p suture (DPS) is likely to be necessary • Antibiotic prophylaxis should be given. Major haemorrhage (See b p.112.) • Common sites of haemorrhage include: external wounds (blood on the floor), intrathoracic, abdominal/retroperitoneal (usually solid organ injury), pelvic fractures (especially ‘open book’), femurs (can lose 1.5 L of blood each), scalp (especially in children). • Diagnostic adjuncts for managing haemorrhage may include US or CT scanning (if the patient is stable enough to go to scan). • Pelvic fractures should be splinted with a pelvic binder. • Femoral fractures should be splinted with longitudinal traction. • Open, or scalp, wounds may require temporary suture. • Use a major haemorrhage protocol (b p.115). • Following initial haemorrhage and hypoperfusion, an acute coagulopathy of trauma can occur; thromboelastography can help guide haemostatic resuscitation with blood coagulation products. • Tranexamic acid may be given (1 g IV bolus followed by 1 g IV over 8 hours). • Correction of hypothermia will improve haemostasis. Intra-abdominal haemorrhage • Intra-abdominal haemorrhage should be suspected in hypotensive victims of major trauma, especially where there is penetrating abdominal trauma, blunt trauma causing external abdominal bruising, signs of peritoneal irritation, haematuria, thoracolumbar fractures, pelvic fractures, or lower rib fractures. • Investigations may include: • Laparotomy (or laparoscopy) • US of abdomen 3 • Diagnostic peritoneal lavage (positive if t100,000 RBC/mm , t500 WBC/mm3, bacteria present on Gram stain) • CT abdomen Traumatic amputation • Major traumatic amputations are particularly seen during ballistic injuries; there is extensive tissue disruption, major bony bleeding, and exposed blood vessels. • Tourniquets applied on-scene at sites proximal to the amputation site can be life saving; they should only be removed by a surgeon as part of damage control surgery.

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Traumatic brain injury (See b p.178.) Traumatic cardiac arrest (See b p.98.) • Cardiac arrest s to trauma has a poor prognosis. • Management involves identifying/treating reversible causes: • Airway obstruction (requiring a definitive airway) • Tension pneumothorax (requiring decompression) • Cardiac tamponade (requiring pericardiocentesis and/or emergency thoracotomy) • Major haemorrhage (requiring haemostasis and resuscitation with blood and blood products)

Further management • Once the patient has been stabilized a s survey should be undertaken (a full history and head-to-toe examination looking for less severe injuries, some of which may still be limb threatening): • Head: • Examine eyes, ears, nose, mouth, scalp, face, cranial nerves • Neck and back (patient usually requires a log roll): • Examine for ‘steps’ or bony tenderness • Anal tone should be tested if spinal injury suspected • May be done early on to remove patient from spinal immobilization boards • Chest, abdomen, and pelvis: • To identify simple pneumothorax, rib fractures, wounds • To monitor for signs of visceral perforation • Review the pelvis X-ray (avoid ‘springing’ the pelvis) • Examination of genitalia • Full skeletal examination, looking for wounds, tenderness, and suspected fractures; X-rays as required. • Check tetanus status. Damage control surgery • Damage control surgery is a combined anaesthetic and surgical concept which involves doing the minimum to the patient required to prevent bleeding and decontaminate wounds. • Once physiology is stabilized, end-organ perfusion restored and acidaemia/temperature/clotting corrected, further staged surgical management may take place. A tertiary survey should be undertaken once the patient has been resuscitated and is finally stabilized on the ward/ICU. On average, 10% of major trauma patients will have a missed injury. Commonly missed issues/injuries include: • A history of comorbid illness. • Eyes: corneal abrasions, contact lenses, vitreoretinal haemorrhage. • Ears: tympanic perforation. • Teeth: dental trauma.

TRAUMA

• Wrist/hands: bony fractures (e.g. metacarpals, scaphoid): • Rings/jewellery should be removed to prevent distal ischaemia and pressure necrosis • Foreign bodies, from the scene or from ED (e.g. caps or bungs which may cause pressure wounds). • Compartment syndrome.

Pitfalls/difficult situations • Missed injuries are common in the first 48 hours. • Nerve damage is often difficult to detect in a sedated patient, a high level of suspicion should be maintained depending upon the mechanism of injury (penetrating/crushing trauma), or associated injuries (fractures/dislocations). • Arterial injury usually presents with a cold, pale, pulseless limb; treatment may involve simply re-aligning a fractured limb, or vascular surgery. • Compartment syndrome is often difficult to detect in sedated patients; a high level of suspicion must be maintained when there are high-risk injuries present (forearm/leg fractures, crush injuries). • The tetanus immunization status of the patient should be established in case a further booster injection is required. • Trauma may be associated with worse outcomes in the elderly, pregnant, malnourished; or those with severe comorbidities. • Increasing inotropic requirements may indicate developing SIRS or occult haemorrhage or injury (e.g. tension pneumothorax). • The signs of an acute abdomen may not be present, especially where a patient has been given neuromuscular blockade for endotracheal intubation and mechanical ventilation. • Medical conditions may coexist with, or cause, trauma, including: • Alcohol intoxication • Syncope/seizures from any cause, especially SAH or cardiac arrhythmias • Diabetic hypoglycaemia

Further reading American College of Surgeons Committee on Trauma. ATLS Guidelines, 8th edn. Chicago, IL: ACS, 2008. Brooks A, et al. Missed injury in major trauma. Injury 2004; 35(4): 407–10. CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet 2010; 376(9734): 23–32. CRASH-2 trial collaborators. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet 2011; 377(9771): 1096–101. Deitch EA, et al. Intensive care unit management of the trauma patient. Crit Care Med 2006; 34(9): 2294–301. Houshian S, et al. Missed injuries in a level 1 trauma centre. J Trauma 52(4): 715–19. Morris CGT, et al. Clearing the cervical spine in unconscious polytrauma victims, balancing risks and effective screening. Anaesthesia 2004; 59: 464–82. Mowery NT, et al. Practice management guidelines for management of hemothorax and occult pneumothorax. J Trauma 2011; 70(2): 510–18. Smith J, et al. Oxford desk reference of major trauma. Oxford: Oxford University Press, 2010.

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3 Drowning Drowning occurs after immersion in liquid resulting in cardiac arrest, or severe injury which may require critical care support. ‘Near-drowning’ is a term which has been used to describe cases who survived.

Causes Drowning is associated with: • Rural/coastal areas (especially where fishing or tourism are prevalent). • Floods. • Drug and alcohol use. • Suicide or assault. • Trauma, hypothermia, coexistent neurological, or cardiac injury. There is little clinical difference between drowning in fresh or salt-water. ‘Dry drowning’ refers to cases where laryngospasm prevents aspiration.

Presentation and assessment • Hypothermia may be present. • Cardiovascular: cardiac arrest may occur, or: • Bradycardia may be present • Severe hypotension may occur due to myocardial dysfunction (s to hypoxia, hypothermia, acidosis, electrolyte abnormalities), or hypovolaemia (associated trauma or fluid shifts) • Respiratory: cough, tachypnoea, dyspnoea, wheeze: • ALI/ARDS may develop (development may be delayed) • Pneumonia may develop • Neurological: anxiety, delirium, coma (s to hypoxia or cerebral oedema). • Metabolic acidosis and lactataemia are common. • Electrolyte abnormalities are rare, but may occur after aspiration of >20 ml/kg water. • Haemolysis, DIC, and AKI can also develop after massive aspiration.

Investigations • • • • • • • • • • •

Core temperature measurement. ABGs (hypoxia, hypercapnia, metabolic acidosis). FBC, coagulation screen, including fibrinogen (DIC). U&Es, LFTs, serum glucose, calcium, magnesium, phosphate, CK. Blood alcohol level (if intoxication suspected). ECG (to identify ischaemia or arrhythmias). CXR (if ALI or pneumonia is suspected). ECHO (if significant CVS instability is present). CT head (if cerebral oedema or infarction suspected). Trauma series X-rays (neck, chest and pelvis, if traumatic injury likely). Consider urine for toxicology (if intoxication suspected).

Differential diagnoses The history of immersion is normally conclusive, but associated injuries may include: hypothermia, trauma, cardiac precipitant (e.g. arrhythmia, MI), neurological precipitant (e.g. epilepsy, stroke, SAH).

DROWNING

Immediate management If the patient is in cardiac arrest follow the guidelines on b p.98 (this may be prolonged if hypothermia is present), otherwise: • Give 100% O2. • If trauma suspected then assume C-spine injury and use collars and spinal stabilization. • Endotracheal intubation may be required for respiratory support or airway protection. • Respiratory support should be provided to maintain O2 saturations of 94–98% (NIV or IPPV may be required). • Fluid resuscitation with/without inotropes may be required to maintain a reasonable perfusion pressure (MAP 65 mmHg): • A CVC may be required to guide fluid resuscitation and allow vasoactive support if required • Continuous ECG monitoring in view of risk of arrhythmias. • Rewarm as appropriate to the degree of hypothermia (b p.252). • Consider inserting an NGT (or OGT if head or facial trauma are present) in order to drain ingested water or debris.

Further management • In comatose patients institute measures to minimize cerebral oedema: • Nurse 15–30° head-up • Treat pyrexia and seizures • Maintain serum glucose of 6–10 mmol/L • If the patient is comatose after resuscitation from cardiac arrest rewarm to 34oC, and maintain at that temperature for 24 hours • Bronchoscopy may be used to remove foreign bodies or debris. • Insert a urinary catheter to monitor urine output. • Consider inserting an arterial line for cardiovascular monitoring and repeated blood gas analyses. • Treat any associated diseases or complications: • Traumatic injuries (b p.404) • Seizures (b p.160) • Cardiac disease and arrhythmias (b pp.98, 132, and 138) • Hypothermia (b p.250) • Hypoglycaemia (b p.234)

Pitfalls/difficult situations • Even where an apparently full recovery has rapidly occurred, patients should be monitored as delayed respiratory compromise may occur. • In paediatric cases consider the possibility of non-accidental injury.

Further reading Carter E, et al. Drowning. Cont Educ Anaesth Crit Care Pain 2011; 11(6): 210–13. Lord SR, et al. Drowning, near drowning and immersion syndrome. J R Army Med Corps 2005; 151: 250–5. Warner DS, et al. Drowning. Update 2009. Anesthesiology 2009; 110: 1390–401.

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4 Severe burns Causes • • • •

Flame/dry heat contact (most commonly in adults). Wet heat contact (scalds, most commonly in children). Electricity (both current-induced injury and flash burns). Chemical damage (rare).

Presentation and assessment Burn thickness may be: • Epidermal (erythematous skin, not counted in % area). • Superficial partial thickness (erythema, clear blisters, blanches). • Deep partial thickness (erythema and white non-blanching areas; bloody blistering). • Full thickness (leathery white or brown skin, painless centre). • Full thickness burn+ (black/charred skin extending to deep structures). Body surface area (BSA) coverage of burns should be assessed at presentation, ideally by a burns team. BSA can be difficult to assess in the initial stages and should be reassessed regularly. Methods include: • Areas of burn equivalent in size to the patient’s palm are ~1% of BSA. • The ‘Rule of 9’s’: • Chest = 18% • Back = 18% • Whole of head = 9% • Whole of arm = 9% (each) • Front of leg = 9% (each) • Back of leg = 9% (each) • Genitalia = 1%. • Lund-Browder charts—these should be used where available. The location of burns is also important: • Airway involvement (see b p.30—singed nasal hair, hoarse voice, soot in airway). • Special areas: head/neck, hands/feet, major joints, chest, perineum. • Circumferential burns: limbs, neck, chest (risk of compartment syndrome, venous obstruction, airway obstruction, or chest restriction). The mechanism of injury/associated trauma should assessed, especially: • Cause of the burn, and duration of exposure to burning agent. • Did the burn occur in an enclosed space (associated with smoke inhalation, airway damage, acute lung injury and CO poisoning)? • Were toxins/accelerants present?

Investigations • • • • • • •

ABGs (hypoxia, metabolic acidosis), COHb by co-oximetry. FBC, coagulation studies, G&S. U&Es, LFTs, serum CK (renal indices and CK may be raised). Toxicology if appropriate. ECG (if feasible). Radiology: CXR, C-spine, pelvis, CT head if indicated. Urine for myoglobin/free Hb.

SEVERE BURNS

Immediate management • • • • • •

Give 100% O2, support airway, breathing, and circulation as required. Use spinal precautions if spinal trauma a possibility. Undertake a p survey and commence resuscitation. Obtain an AMPLE history (b p.2). Keep patients NBM. Alert the burns/plastics team.

Airway (See also b p.30 for inhalational injuries.) • Early endotracheal intubation is likely to be necessary where: • GCS 8 or rapidly decreasing • Burns are widespread (>30% BSA) • There is facial or airway involvement • Use an uncut oral tube to allow for facial swelling. • Suxamethonium is safe to use in the immediate setting (unless there are other contraindications). Breathing • Ventilatory support may be required. • Consider the possibility of associated chest trauma. • Circumferential chest burns may require surgical escharotomy. • Raised COHb levels will require 100% FiO2 until COHb 5% full thickness burn. • Burn to hands, feet, genitalia, perineum, joints. • Burns to face. • Electrical/chemical burns. • Circumferential burns (limbs or chest). • Extremes of age. To a burns ICU • Burns affecting >30% BSA. • Burns affecting upper chest, neck, or face (affecting airway). • Burns affecting the airway. • Smoke inhalation. • COHb >20%. • s complications (e.g. sepsis, renal failure, major trauma).

Pitfalls/difficult situations • Do not assume that patients have been adequately assessed or resuscitated prior to ICU admission, especially following inter-hospital transfers. • Airway protection: if in doubt intubate—delay may make a difficult intubation impossible. • Do not use suxamethonium >48 hours or 60% have a high mortality, especially if associated with inhalation injury. • Traditional prediction models overestimate mortality from burn injury.

Further reading Hettiaratchy S, et al. Initial management of a major burn: I-overview Br Med J 2004; 328: 1555–7. Ipaktchi K, et al. Advances in burn critical care Crit Care Med 2006; 34(9): S239–S244. Treharne LJ, et al. The initial management of acute burns J R Army Med Corps 2004; 15B0: 74–81.

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4 Electrocution Electrical injury can disrupt the normal electrical function of cells (e.g. causing arrhythmias or muscle tetany), or cause internal and external burns. Other injuries may result from muscle damage or contraction.

Causes Contact with electrical sources can result in electrical injuries. The current involved is the major determinant of tissue damage. • Lightning (immediate, ultra-high voltage and current, DC). • High voltage (short-lived, >1000 V, high current, AC or DC). • Low voltage (may be prolonged, 90 mmHg (on 2 separate occasions); with proteinuria of 0.3 g in a 24-hour period. Severe pre-eclampsia is defined as pre-eclampsia with a systolic BP >160 mmHg or diastolic BP >110 mmHg and/or symptoms (e.g. altered neurology), and/or biochemical/haematological impairment. Death occurs as a result of CVA, hepatic failure, cardiac failure, or pulmonary complications. Eclampsia is the occurrence of major seizure activity in the presence of pre-eclampsia (38% occur antepartum, 18% intrapartum, 44% postpartum). It may occur before the signs of hypertension or proteinuria.

Causes Risk factors for pre-eclampsia include: • First pregnancy. • Pre-eclampsia in a previous pregnancy. • A family history of PIH or PET. • Diastolic BP >80 mmHg at booking. • Obesity. • Increasing maternal age. • Multiple pregnancies or polyhydramnios. • Underlying medical conditions: • Previous hypertension • Diabetes mellitus • Renal disease • Autoimmune disease such as SLE or antiphospholipid antibodies

Presentation and assessment Pre-eclampsia, even when severe, may be asymptomatic and only discovered by routine blood pressure screening, or when complications such as eclampsia occur. Signs and symptoms, when they occur, consist of: • Neurological: • Headache and/or visual disturbance (cerebral oedema) • Hyper-reflexia/clonus (t3 beats) • Seizures • Papilloedema • Respiratory: • Dyspnoea on exertion • Pulmonary oedema • ALI, ARDS • Cardiovascular: hypertension (>140/90 mmHg). • GI: • Nausea and vomiting; • Epigastric discomfort (hepatic engorgement/ischaemia) • Renal: proteinuria, marked oliguria (often 10 x the gestational age in weeks in μmol/L, or >360 μmol/L, or >6 mg/dL). • Urinalysis, options include: • Urine dipstick (proteinuria: t++ seen; severe proteinuria: t+++ seen); t+ proteinuria seen requires further investigation • Spot protein: creatinine ratio (PCR) >30 mg/mmol • 24-hour collection (proteinuria: t0.3 g/24 hours; severe proteinuria: >1 g/24 hours) • Blood, urine, and sputum cultures (if infection is suspected). • US of the fetus, to examine for fetal well-being.

Differential diagnoses • Seizures or altered neurology: • Epilepsy (prior history of seizures) • Encephalitis/meningitis (signs of sepsis) • CVA (CT findings, absence of proteinuria) • HUS/TTP (evidence of haemolysis) • Hypertension: • Pre-existing hypertension (prior history) • Pain/agitation

Immediate management A multidisciplinary approach should be adopted with input from senior critical care/anaesthetic, obstetric, and midwifery disciplines • Give O2 and support airway, breathing, and circulation as required. • Overall aims include stabilization of BP, prevention of eclamptic seizures, and opportune delivery of the baby. Hypertension treatment • The aim should be to reduce diastolic BP to around 90–100 mmHg, precipitous drops in BP should be avoided. • There is no consensus as to what constitutes first- or second-line therapy, a reasonable approach might be:

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•

•

•

•

Obstetric and fertility patients

First-line treatment: labetalol 200 mg PO, repeated after 30 minutes if required; if oral labetalol is ineffective consider labetalol 50 mg IV repeated every 5 minutes to a maximum of 200 mg, followed by infusion at 5–50 mg/hour Second-line: if labetalol is not tolerated or contraindicated (e.g. in asthmatics) give nifedipine 10 mg PO, which can be repeated after 30 minutes if required (nifedipine should not be given sublingually) Third-line: hydralazine 5–10 mg by slow IV bolus, repeated after 15 minutes, followed by an infusion at 5–15 mg/hour (consider a bolus of d500 ml crystalloid before, or at the same time as hydralazine given in the antenatal period) Atenolol, ACE inhibitors, ARBs, and diuretics should be avoided

Treatment and/or prevention of eclamptic seizures • Magnesium sulphate IV 4 g (16 mmol MgSO4) over 5–10 minutes, followed by an infusion of 1 g/hour (4 mmol/hour) for at least 24 hours: • A further dose of magnesium sulphate 2 g (8 mmol MgSO4) over 15–20 minutes can be given if further seizures occur; or the infusion rate i to 2 g/hour • Close observation for evidence of magnesium toxicity is essential (see b p.224). • Second-line eclampsia treatments are only rarely required if BP control and magnesium have been used, but may include: • IV phenytoin or benzodiazepines (b p.161) • Induction of anaesthesia with endotracheal intubation and ventilation (the presence of upper airway oedema suggests difficult intubation will be more likely) • The definitive treatment for severe pre-eclampsia/eclampsia is delivery of the baby: • The decision to deliver must weigh up the needs of the mother against the maturity of the baby • Seizures and other symptoms should be controlled prior to proceeding to delivery/Caesarean section if possible • Consider IV steroids for fetal lung development (b p.427) • Patients may be transferred to critical care for enhanced monitoring and vital organ support pre- or post-delivery

Further management • The role of CVP monitoring is unclear, it can aid fluid management, but is not always required if urine output/fluid balance is strictly monitored; it is more difficult in the presence of agitation, dyspnoea, oedema, and coagulopathy. • There is no evidence of benefit from fluid expansion and a fluid restriction regimen is associated with good maternal outcome: • Limit maintenance fluids to 80 ml/hour unless there are other ongoing fluid losses, such as haemorrhage • There is no evidence that maintenance of a specific urine output is important to prevent renal failure (which is rare).

SEVERE PRE-ECLAMPSIA/ECLAMPSIA

Pitfalls/difficult situations • Endotracheal intubation may cause a profound hypertensive surge; short-acting IV opiates, or IV antihypertensives such as labetalol, should be used to blunt this effect. • Up to 10% of women with severe pre-eclampsia, and 25–50% of women with eclampsia are affected by the HELLP syndrome. • The key issue picked up in recent ‘Confidential Enquiries’ is the need to adequately treat BP; systolic BP >150 mmHg with pre-eclampsia should be treated to protect the maternal brain.

Further reading Altman D, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo- controlled trial. Lancet 2002; 359: 1877–890. Duley L, et al. Management of pre-eclampsia. Br Med J 2006; 332; 463–468. NICE. Hypertension in pregnancy: the management of hypertensive disorders during pregnancy. London: NICE, 2011.

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3 HELLP syndrome HELLP syndrome consists of Haemolysis, Elevated Liver enzymes, and Low Platelets. It may occur as an entity on its own, or in association with pre-eclampsia. The associated mortality is reported to be as high as 24% of patients.

Causes HELLP is a multisystem disease consisting of generalized vasospasm and coagulation defects. No common precipitating factor has been identified. • Haemolysis is due to a microangiopathic haemolytic anaemia (MAHA). • Elevated Liver enzymes are due to hepatic necrosis (in severe cases intra-hepatic haemorrhage, subcapsular haematoma or hepatic rupture may occur). • Low Platelets/thrombocytopaenia is due to iconsumption.

Presentation and assessment The signs and symptoms overlap with those of pre-eclampsia: • Neurological: headache and/or visual disturbance (cerebral oedema), hyper-reflexia/clonus, seizures. • Respiratory: dyspnoea on exertion, pulmonary oedema, ALI/ARDS. • Cardiovascular: hypertension (>160/110 mmHg). • GI: right upper quadrant tenderness, nausea and vomiting, epigastric discomfort (hepatic engorgement/ischaemia). • Renal: proteinuria, marked oliguria (often 40 x 10 /L are unlikely to bleed • Transfusion is generally only required if the platelet count drops to less than 20 x 109/L • Patients who undergo Caesarean section should be transfused to a platelet count >50 x 109/L • Patients with DIC should be given FFP and packed RBCs. • See also section on pre-eclampsia management (b p.432). • Seizure prophylaxis: magnesium sulphate should be administered to prevent seizures, regardless of whether hypertension is present. • Antihypertensives: should be administered according to the protocol for pre-eclampsia. • Fluids: as for pre-eclampsia. • If required betamethasone should be given to promote fetal lung maturation (b p.427).

Further management • Consider plasmapheresis after delivery. • Epoprostenol and ketanserin have also been used as treatments.

Pitfalls/difficult situations • Postpartum haemorrhage will require aggressive early treatment. • High-dose steroids are no longer recommended as a treatment for HELLP.

Further reading Haram K, et al. The HELLP syndrome: clinical issues and management. A review. BMC Pregnancy Childbirth 2009; 9: 8. Hart E, et al. The diagnosis and management of pre-eclampsia. BJA CEPD Rev 2003; 3(2): 38–42.

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4 Anaphylactoid syndrome of pregnancy Anaphylactoid syndrome of pregnancy, also known as amniotic fluid embolism (AFE), is thought to be caused by amniotic fluid entering the maternal circulation, triggering an anaphylactoid reaction and/or DIC.

Causes Risk factors include induction of labour and multiple pregnancy; older age and increasing parity may also be associated. It can occur at any time in late pregnancy, during or after labour/delivery (by vaginal delivery or Caesarean section), and also after termination.

Presentation and assessment Anaphylactoid syndrome of pregnancy presents as collapse during labour or delivery (or within 30 minutes of delivery) with acute hypotension, respiratory distress and acute hypoxia. Presentation is typically biphasic. Phase 1 signs/symptoms • Dyspnoea, tachypnoea, pulmonary oedema, hypoxia, cyanosis: • Pulmonary hypertension and right heart failure (s to pulmonary artery vasospasm/obstruction) • Cardiovascular: hypotension, cardiovascular collapse, cardiac arrest. • Neurological: tonic–clonic seizures. • Other: fetal bradycardia. Up to half of the survivors of phase 1 enter phase 2 • DIC with massive haemorrhage s to the coagulopathy (may occur as the presenting feature, without phase 1 features).

Investigations • ABGs (acidaemia, hypoxia, hypercapnia). • Crossmatch, FBC. • Coagulation studies, including fibrinogen (DIC may occur with raised PT and APTT, thrombocytopaenia, hypofibrinogenaemia). • U&Es, LFTs, serum glucose (exclude hypoglycaemia). • Serum tryptase (if anaphylaxis suspected, see b p.110). • 12-lead ECG and/or cardiac echocardiography (differentials include cardiac ischaemic, arrhythmias; right-sided strain in PE). Once the patient has been stabilized: • CT pulmonary angiogram, or VQ scan (if PE suspected). • CT head may be required. • If a PAFC has been inserted a pulmonary artery blood sample may be examined for fetal cells or amniotic fluid (a finding associated with, but not diagnostic of, the syndrome); urine may also be examined.

Differential diagnoses All differentials will be difficult to exclude/confirm in the acute situation: • Occult haemorrhage (e.g. placental abruption, uterine rupture). • Anaphylaxis (triad of hypotension, bronchospasm, and urticarial rash). • PE (pleuritic chest pain and respiratory distress). • Aortic dissection (tearing chest pain and hypotension).

ANAPHYLACTOID SYNDROME OF PREGNANCY

• MI (crushing chest pain and hypotension). • Septic shock (pyrexia and vasodilatory shock). • Local anaesthetic toxicity, or regional anaesthesia complications.

Immediate management A multidisciplinary approach should be adopted with input from senior critical care/anaesthetic, obstetric, and midwifery disciplines • Give O2 and support airway, breathing, and circulation as required • Intubation and mechanical ventilation is often required: • NIV support may be considered in some cases • Aggressive fluid resuscitation with vasopressor/inotropic support is likely to be required for haemodynamic instability. • Anaphylaxis is often difficult to exclude, treatment with adrenaline, steroids, and antihistamine may be required (b p.110). • Seizures occur as a result of cerebral anoxia and should be treated according to the protocol for status epilepticus (b p.160), with benzodiazepines as first line agent), except: • If eclampsia is a likely differential diagnosis consider using magnesium sulphate (see b p.434) as the first line agent (eclampsia is associated with hypertension; anaphylactoid syndrome of pregnancy is associated with hypotension, which will be exacerbated by magnesium) • The fetus should be delivered as soon as is practically possible to prevent further hypotensive episodes. • If phase 1 is survived then transfer to critical care for close monitoring and vital organ support is likely to be required. • Early invasive monitoring is advised. • The coagulopathy/DIC which occurs in phase 2 should be corrected: • Packed red cells, platelets, FFP, and cryoprecipitate are all likely to be required • ARDS commonly develops; a lung protective ventilation strategy should be adopted.

Further management • Haemodialysis with plasmapheresis, and extracorporeal membrane oxygenation with IABP support have both been described in case reports with successful outcomes in treating anaphylactoid syndrome patients with cardiovascular collapse.

Pitfalls/difficult situations • Until recently maternal mortality was thought to be 50–75%, more recent estimates of mortality are around 20%, although those who do survive are often left with significant neurological disability.

Further reading Conde-Agudelo A, et al. Amniotic fluid embolism: an evidence-based review. Am J Obs Gynaecol 2009; 201(5): 445.e1–13. Knight M, et al. Incidence and risk factors for amniotic-fluid embolism. Obstet Gynaecol 2010; 115(5): 91091–7. O’Shea A, et al. Amniotic fluid embolism. Int Anesthesiol Clin 2007; 45(1): 17–28.

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3 Massive obstetric haemorrhage Major obstetric haemorrhage is defined as 1 or more of the following: • Estimated blood loss t2000 ml.1 • Transfusion of 5 or more units of blood. • 50% blood volume loss within 3 hours. • Rate of blood loss t 150 ml/minute. • Blood loss precipitating treatment for coagulopathy (e.g. FFP, cryoprecipitate, platelets). Haemorrhage may be antepartum (APH), occurring before delivery but after 24 weeks’ gestation, or postpartum (PPH) occurring during or after delivery.

Causes • • • • • • • • • •

Ectopic pregnancy. Placental abruption. Placenta praevia. Sepsis: septic abortion or puerperal sepsis. Uterine atony. Placenta accreta. Uterine/cervical/vaginal trauma. Uterine rupture. Retained products of conception. Coagulopathy, especially DIC.

Presentation and assessment The definition of massive haemorrhage assumes that >20–30% of total blood volume has already been lost. The presentation is similar to haemorrhage from other causes (b p.112), and includes: • Respiratory: dyspnoea, tachypnoea. • Cardiovascular: • Tachycardia (may be obtunded by regional anaesthesia; bradycardia is generally a late/pre-terminal sign) • Delayed capillary refill, hypotension • Renal: oliguria/anuria. • Neurological: anxiety, thirst, drowsiness or unconsciousness. • Other: pallor. Bleeding PV or from the Caesarean section wound (or into the postoperative drains) may be seen. Occasionally bleeding is occult (e.g. uterine rupture, placental abruption, or postnatal vaginal or round ligament haematoma); abdominal pain may be present. • Fetal CTG or blood gases may be abnormal.

Investigations • ABGs (metabolic acidosis with/without respiratory compensation). • FBC (dhaemoglobin; thrombocytopaenia in DIC). • Coagulation studies, including fibrinogen (DIC may occur with raised PT and APTT, thrombocytopaenia, hypofibrinogenaemia). 1

Blood loss may be difficult to estimate as it may be mixed with amniotic fluid during delivery.

MASSIVE OBSTETRIC HAEMORRHAGE

• U&Es, LFTs. • Serum calcium (dwith massive transfusion). • Where bleeding is associated with suspected concealed pregnancy, β-HCG (urine or blood) or abdominal US may aid the diagnosis.

Differential diagnoses • Anaphylactoid syndrome of pregnancy (dyspnoea, shock, possible seizures). • Anaphylaxis (hypotension, bronchospasm and urticarial rash). • Sepsis (pyrexia and vasodilatory shock). • Vasovagal response (to uterine stimulation, causing profound bradycardia). • Local anaesthetic toxicity, or regional anaesthesia complications.

Immediate management A multidisciplinary approach should be adopted with input from senior critical care/anaesthetic, obstetric, midwifery, and haematology disciplines and the blood bank (Fig. 13.3): • Give O2 and support airway, breathing, and circulation as required. • Intubation and mechanical ventilation are likely to be required, and will facilitate any surgery. • Use the left lateral position or a wedge, to avoid aortocaval compression. • Aggressive fluid resuscitation is required (warmed fluids if possible): • Accurate estimation of blood loss is essential • Large-bore IV cannulae will be required for rapid fluid infusion • Early packed red cell transfusion is likely to be needed, with O-negative blood if required • The use of bedside/portable Hb monitoring will guide transfusion • Consider cell salvage if trained staff and equipment available • Invasive monitoring, particularly CVP monitoring, may be required • Ensure prompt recognition and aggressive treatment of coagulopathies: • Transfuse FFP, cryoprecipitate, and platelets as required • Consider vitamin K • Liaise with haematologists • Repeatedly check coagulation screen and fibrinogen • Consider recombinant factor VIIa for severe uncontrolled coagulopathy (see b Pitfalls/difficult situations) • Postpartum uterine atony may respond to: • Manual massage/bimanual compression • Oxytocin (5 units IV slow bolus, followed by an infusion at 10 units/hour) • Followed by ergometrine 500 mcg IM (unless there is a history of hypertension) • Additional agents include carboprost 250 mcg IM or intrauterine (non-licensed route of administration, avoid in asthmatics), every 15 minutes up to a maximum of 8 doses; or misoprostol 1000 mcg rectally

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• Available surgical treatments depend upon the cause of the bleeding (see also b Pitfalls/difficult situations, b p.442) and include: • Traumatic tears may be repaired • Retained products of conception or retained placenta may be removed • Bleeding from placental site (e.g. placenta praevia) may respond to pressure from balloon tamponade • Uterine atony may respond to a brace suture (B Lynch), internal iliac artery ligation, hysterectomy or radiological intervention (e.g. angiographic embolization) • Temporary aortic compression may ‘buy time’

Further management • Postoperative monitoring should be in a critical care environment, ideally including arterial and CVP monitoring. • Coagulopathy/DIC, clotting factor deficiency, or thrombocytopaenia may require treatment with platelets, FFP, or cryoprecipitate: • Where possible treatment should be guided by haematology • Other complications of massive haemorrhage may include: • Hypothermia requiring active warming via a warm air blanket and warmed IV fluids (re-warming will also improve the efficacy of clotting factors) • Transfusion related acute lung injury (TRALI) may require support with non-invasive CPAP or ventilation; or with mechanical ventilation with a lung protective strategy • AKI: renal support may require volume resuscitation, maintenance of adequate perfusion pressure, or even renal replacement therapy • Hyperkalaemia (consider giving insulin/dextrose, or salbutamol) • Hypocalcaemia requiring calcium replacement if resistant hypotension is present

Pitfalls/difficult situations • Recurrent haemorrhage can prove difficult to control, options include: • Returning to theatre for further surgical interventions • Further aggressive correction of coagulopathy • Recombinant factor VIIa (the use of recombinant factor VIIa in haemorrhage is an unlicensed indication with disputed efficacy) • Angiographic embolization • Regional anaesthesia may ‘hide’ abdominal pain associated with concealed bleeding such as uterine rupture. • The increase in circulating blood volume which occurs in pregnancy may delay the onset of symptoms associated with haemorrhage.

Further reading Banks A, et al. Massive haemorrhage in pregnancy. Cont Educ Anaesth Crit Care Pain 2005; 5(6) 195–8. RCOG. Blood transfusion in obstetrics. London: Royal College of Obstetricians and Gynaecologists. Green-top Guideline No. 47, 2007. RCOG. Prevention and management of postpartum haemorrhage. London: Royal College of Obstetricians and Gynaecologists. Green-top Guideline No. 52, 2009.

MASSIVE OBSTETRIC HAEMORRHAGE

Resucitation, monitoring, investigation and treatmentshould occur simultaneously Major obstetric haemorrhage Blood loss > 1000 ml Continuring major obstetric haemorrhage or clinical shock

Call for help Senior midwife/obstetrician and anaesthetist Alert haematologist Alert blood transfusion laboratory Alert consultant obstetrician on-call

Resuscitation Airway Breathing Circulation Oxygen mask (15 litres) Fluid balance (2 litres Hartmann’s, 1.5 litres colloid) Blood transfusion (O RhD negative or group-specific blood) Blood products (FFP, PLT, cryoprecipitate, factor Villa) Keep partient warm

Monitoring and investigations 14-g cannulae × 2 FBC, coagulation, U&Es, LFTs Crossmatch (4 units, FFP, PLT, cryoprecipitate) ECG, oximeter Faley catheter Hb bedside testing Blood products Consider central and arterial lines Commence record chart Weigh all swabs and estimate blood loss

Medical treatment Bimanual uterine compression Empty bladder Oxytocin 5 iu x2 Ergometrine 500 micrograms Oxytocin infusion (40 iu in 500 ml) Carboprost 250 micrograms IM every 15 minutes up to 8 times Carboprost (intramyometrial) 0.5 mg Misoprostol 1000 micrograms rectally

Theatre Is the uterus contracted? Examination under anaesthesia Has any clotting abnormality been corrected?

Intrauterine balloon tamponade Brace suture Consider interventional rediology

Surgery

Bilateral uterine artery ligation Bilateral internal iliac ligation Hysterectomy (second consultant) Uterine artery embolisation

Consider high-dependency unit or intensive care unit

Fig. 13.3 Major postpartum haemorrhage algorithm. Royal College of Obstetricians and Gynaecologists. Prevention and management of postpartum haemorrhage. Green-top Guideline No. 52, 2009. Reproduced with kind permission from the RCOG.

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3 Ovarian hyperstimulation syndrome Ovarian hyperstimulation syndrome (OHSS) is an unusual complication of medicines that stimulate egg production as part of fertility treatment.

Causes All women undergoing ovarian stimulation therapy should be considered at risk of OHSS. Higher risk categories of women include: • Women with polycystic ovaries. • Aged 12 cm1 OHSS tense ascites or large hydrothorax Haematocrit >55% WCC >25 x 109/L Severe oliguria/anuria Thromboembolism Acute respiratory distress syndrome

1 Ovarian size may not correlate with severity of OHSS in cases of assisted reproduction because of the effect of follicular aspiration. Reproduced from: Royal College of Obstetricians and Gynaecologists. Management and prevention of ovarian hyperstimulation syndrome (OHSS). Green-top Guideline No. 5. London: RCOG; 2006, with the permission of the Royal College of Obstetricians and Gynaecologists.

Presentation and assessment OHSS typically occurs 1–2 days after follicular rupture/aspiration; only 5% of OHSS cases are moderate severity or worse. The features of OHSS are described in the classification of severity, but may also include: • General: pyrexia (infection commonly occurs alongside OHSS). • Cardiorespiratory: hypotension, tachycardia, pulmonary oedema. • Renal: metabolic acidosis, hyperkalaemia hyponatraemia, AKI.

OVARIAN HYPERSTIMULATION SYNDROME

Investigations • • • • • • • • • • •

Measure weight and abdominal girth on admission, and daily thereafter. Abdominal/vaginal US (ascites, ovarian size). ABGs (metabolic acidosis). FBC (raised haematocrit; raised WCC), coagulation studies. U&Es (raised urea/creatinine; dNa may be seen in up to 50% of cases). LFTs (abnormal in up to 40%, but improve with disease resolution). Serum glucose, serum CRP. Blood, sputum, urine cultures (if infection suspected). CXR (basal atelectasis/pneumonia, pleural effusion, ALI/ARDS). ECG/ECHO (if pericardial effusion suspected). CTPA or VQ scan (if PE suspected).

Differential diagnoses Several diseases may mimic OHSS, or coexist with it (e.g. acute abdomen, or intra-abdominal haemorrhage; PE or pneumonia).

Immediate management A multidisciplinary approach should be adopted with input from senior critical care/anaesthetic, obstetric and midwifery disciplines: • Give O2 and support airway, breathing, and circulation as required. • The rapid development of abdominal distension and ARDS may necessitate endotracheal intubation and mechanical ventilation: • In women requiring invasive respiratory support, a lung-protective strategy should be used (b p.53) • Hydrothorax may require drainage if present • Women with severe haemoconcentration (Hb >14 g/dL, Hct >45%) will need intensive initial rehydration with 0.9% saline and/or colloid: • Potassium-containing solutions should be avoided due to the potential for hyperkalaemia • Invasive monitoring is indicated for severe OHSS with oliguria and haemoconcentration despite colloid volume expansion • IAP should be monitored closely: • IAP >20 mmHg suggests the need for decompression • Consider (US-guided) paracentesis where: • Abdominal distension is severe or impairs respiratory function • Oliguria persists despite adequate volume replacement • IV fluid replacement should be considered in women who have large volumes of ascites drained (hypotension may occur).

Further management • Thromboprophylaxis should be provided as there is a high risk of PE. • Hyponatraemia should be corrected. • Pelvic surgery should be restricted to cases with coincident problems requiring surgery or adnexal torsion (suspected if there is further ovarian enlargement, worsening unilateral pain, nausea, leucocytosis and anaemia; Doppler ultrasonography may help to diagnose torsion).

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• Consider empirical antibiotic treatment, if infection is suspected, e.g. piptazobactam IV 4.5 g 8-hourly and gentamicin IV 5 mg/kg daily. • Diuretics are generally avoided as they deplete intravascular volume; they may have a role with careful haemodynamic monitoring in cases where oliguria persists despite adequate intravascular volume expansion and a normal IAP.

Pitfalls/difficult situations • Unusual neurology should raise the possibility of a thrombotic episode in an uncommon location.

Further reading Budev MM, et al. Ovarian hyperstimulation syndrome. Crit Care Med 2005; 33(10): S301–306. RCOG. The management of ovarian hyperstimulation syndrome. London: Royal College of Obstetricians and Gynaecologists, Green top Guideline No. 5, 2006.

Chapter 14

Poisoning and overdose Emergency management 448 Analgesics 460 Antidepressants 466 Sedatives 472 Inhaled poisons 476 Industrial chemicals 480 Alcohols and hydrocarbons 482 Recreational drugs 486 Miscellaneous poisons 490

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3 Emergency management Poisoning or overdose (OD) may be intentional or unintentional. It can occur via ingestion, injection, or inhalation, and rarely by transdermal or other routes. It may be obvious from the history and presentation, but a high index of suspicion may also be required. The emergency management of poisoning involves: • Initial resuscitation. • Identification, where possible, of likely agent. • Specific treatments or antidotes. • General supportive measures.

Causes Common poisoning agents include: • Pharmaceutical products including ‘over-the-counter medications’: • E.g. paracetamol (and paracetamol-containing products), aspirin (and other analgesics/NSAIDs), opiates/opioids, benzodiazepines and ‘Z-drugs’ (e.g. zopiclone), antidepressants (including SSRIs and tricyclics), and barbiturates • Recreational drugs (including alcohol, the most common drug to be co-ingested either with recreational drugs or as part of self-poisoning): • E.g. opiates/opioids, cocaine, amphetamines, ecstasy, gammahydroxybutyric acid (GHB), hallucinogenics (e.g. LSD), glues or volatile chemicals • Industrial chemicals, household chemicals, and environmental toxins including inhaled poisons (e.g. carbon monoxide and cyanide): • E.g. organophosphates, paraquat, methanol, ethylene glycol, household products (e.g. batteries, cleaning agents and detergents) • Animal, fish, and insect bites/stings.

Presentation and assessment • A history of attempted suicide, psychiatric illness, or substance abuse. • Airway or respiratory signs and symptoms: • Respiratory depression • Aspiration, pneumonitis, or bronchospasm • Oropharyngeal burns • Cardiovascular: • Hypotension, hypertension, cardiovascular collapse, cardiac arrest • ECG: tricyclics and antidepressants, amongst other drugs, cause conduction defects and arrhythmias, which may be resistant to treatment • Neurological: • Agitation, confusion, or hallucinations • Unexplained unconsciousness, especially if associated with compartment syndrome or prolonged contact burns • Convulsions • Profound weakness, or conversely muscle rigidity or dystonia • Ataxia or nystagmus • GI: vomiting or diarrhoea; liver failure. • Renal: renal failure, rhabdomyolysis.

EMERGENCY MANAGEMENT

Other features that may be associated with poisoning include: • Hypo- or hyperthermia. • Self-harm injuries. • Trauma, burns, drowning, and head injuries. • Electrolyte imbalance, especially sodium, potassium, or glucose. • Metabolic acidosis, especially with a raised osmolar or anion gap (see b p.205). Individual signs and symptoms are associated with certain poisons (Tables 14.1–14.4). Clusters of symptoms may occur together when poisoning with certain agents has occurred; these are commonly referred to as ‘toxidromes’ (Table 14.5).

Investigations The investigations required will be dictated by the patient’s severity of illness, and the most likely causative agent(s), but may include: • ABGs (hypoxia, hypercapnia, metabolic acidosis, raised anion gap). • FBC, coagulation studies (coagulation may be deranged). • Blood methaemaglobin concentration (see b p.453). • RBC cholinesterase activity (in organophosphate poisoning). • U&Es, LFTs. • Serum calcium (in ethylene glycol poisoning) and phosphate. • Serum CK (raised in rhabdomyolysis). • Serum glucose. • Blood alcohol levels (or expired air levels if possible). • Paracetamol and salicylate levels (important to check timings). • Specific drug serum levels may be indicated for other substances (e.g. ethylene glycol, digoxin, valproic acid, phenytoin, theophylline, iron, lithium, carbamazepine). • Carboxyhaemoglobin (by co-oximetry). • Urine for myoglobin. • Consider taking blood, urine, and gastric aspirate samples for toxicology, or for storage in case later analysis is required. • 12-lead ECG (may show ischaemia, evidence of hyperkalaemia or QT prolongation). • CXR (if aspiration suspected or prior to hyperbaric oxygen therapy). • AXR may be useful if ingestion of radiopaque substances is suspected (chloral hydrate, heavy metals, iron, enteric coated or sustained release preparations, ‘body packing’). • Consider head CT or LP to exclude other causes of unconsciousness.

Differential diagnoses • Conditions causing altered consciousness, altered behaviour, or respiratory depression (e.g. head injuries, meningitis/encephalitis, hypoglycaemia and post-ictal state). • Conditions causing cardiovascular collapse (e.g. anaphylaxis). • Conditions causing muscle weakness (e.g. Guillain–Barré and botulism) • Conditions causing non-specific symptoms such as vomiting or hypothermia (e.g. infections/sepsis, neurological injury/SAH).

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Table 14.1 Cardiorespiratory changes and associated poisons Signs and symptoms

Potential poisons

Respiratory depression; hypoventilation

Alcohols, barbiturates, benzodiazepines, botulinum toxin, neuromuscular blocking agents, opioids, sedatives, strychnine, tranquillizers, tricyclic antidepressants

Tachypnoea

Ethylene glycol, isoniazid, methanol, pentachlorophenol, salicylates

Pulmonary oedema

Cocaine, chlorophenoxy herbicides, ethylene glycol, hydrocarbons, irritant gases, organic solvents, opioids, paraquat, phosgene, salicylates

Pneumothorax

Cocaine

Bradycardia

β-blockers, calcium-channel antagonists, carbamates, cholinergics, clonidine, digoxin, lithium, metoclopramide, opioids, organophosphates, phenylpropanolamine, physostigmine, propoxyphene, quinidine

Tachycardia

Amphetamines, anticholinergics, antihistamines, caffeine, carbon monoxide, cocaine, cyanide, hydralazine, hydrogen sulphide, phencyclidine, phenothiazines, sympathomimetics, theophylline, thyroxine, tricyclic antidepressants

Arrhythmias

β-blockers, chloroquine, cyanide, digoxin, phenothiazines, quinidine, theophylline, tricyclic antidepressants

Hypotension

β-blockers, calcium channel antagonists, ethanol, opioids, sedatives, tranquillizers

Hypertension

Anticholinergics, sympathomimetics

Table 14.2 Temperature, skin, and oral changes Signs and symptoms

Potential poisons

Hyperthermia

Anticholinergics, amphetamines, antihistamines, cocaine, dinitrophenols, hydroxybenzonitriles, LSD, MAOIs, phencyclidine, phenothiazines, pentochlorophenols, procainamide, quinidine, salicylates, tricyclic antidepressants

Hypothermia

Barbiturates, carbon monoxide, colchicine, ethanol, lithium, opioids, phenothiazines, sedatives, tricyclic antidepressants

Excess salivation

Cholinesterase inhibitors, strychnine

Dry mouth

Anticholinergics, opioids, tricyclic antidepressants, phenothiazines

Sweating

Cholinergics, hypoglycaemics, sympathomimetics

Dry skin

Anticholinergics

Hair loss

Thallium

Acne

Bromide, organochlorine

EMERGENCY MANAGEMENT

Table 14.3 Neurological and eye changes Signs and symptoms

Potential poisons

Coma, dconsciousness

Alcohols, benzodiazepines, barbiturates, bethanechol, carbamates, clonidine, GHB, hypoglycaemic agents, lithium, nicotine, opioids, organophosphates, physostigmine, pilocarpine, salicylates, tranquillizers tricyclic antidepressants

Convulsions

Amphetamines, anticholinergics, antihistamines, antipsychotics, caffeine, camphor, carbamates, carbon monoxide, chlorinated hydrocarbons, cocaine, ethylene glycol, isoniazid, lead, lidocaine, lindane, lithium, methanol, nicotine, organophosphates, orphenadrine, phencyclidine, propranolol, salicylates, strychnine, theophylline, tricyclic antidepressants

Paraesthesia

Thallium

Ataxia/nystagmus Antihistamines, bromides, barbiturates, carbamazepine, carbon monoxide, diphenylhydantoin, ethanol, phenytoin, piperazine, sedatives, thallium Miosis

Barbiturates, carbamates, cholinergics, clonidine, ethanol, isopropyl alcohol, organophosphates, opioids, phencyclidine, phenothiazines, physostigmine, pilocarpine

Mydriasis

Amphetamines, anticholinergics, antihistamines, cocaine, dopamine, glutethimide, LSD, MAOIs, phencyclidine, tricyclic antidepressants

Blindness

Quinine, methanol

Table 14.4 Gastrointestinal and renal changes Signs and symptoms

Potential poisons

Vomiting

Aspirin, iron, fluoride, theophylline

GI bleed

Anticoagulants, corrosive compounds, NSAIDs, salicylates

Liver failure

Carbon tetrachloride, paracetamol

Diarrhoea

Arsenic, cholinesterase inhibitors

Constipation

Lead, opioids, thallium

Urinary retention

Atropine, opioids, tricyclic antidepressants

Incontinence

Carbamates, organophosphates

Crystals in urine

Ethylene glycol, primidone

Renal failure

Amanita toxin, aminoglycosides, cadmium, carbon tetrachloride, ethylene glycol, oxalates, paracetamol, polymyxin, mercury, methanol.

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Table 14.5 Toxidromes and combinations of symptoms and the likely associated poisons Toxidromes

Constellation of signs and symptoms

Possible toxins

Anticholinergic activity

Agitation, delirium, diminished consciousness, mydriasis hyperthermia, dry skin and mucosal membranes, flushing, tachycardia, bowel stasis, urinary retention

Anticholinergic alkaloids (e.g. in plants such as belladonna), antihistamines, antiparkinsonian drugs, atropine, baclofen, cyclopentolate, phenothiazines, propantheline, scopolamine, tricyclic antidepressants

Cholinergic activity (muscarinic and/or nicotinic effects)

Miosis or mydriasis, blurred vision, sweating, excess salivation, lacrimation or bronchial secretions, wheezing or dyspnoea, tachycardia or bradycardia, hypertension, vomiting and diarrhoea, abdominal cramps, urinary and faecal incontinence, muscle weakness, fasciculations, paralysis

Acetylcholinesterase inhibitors: carbamates, neostigmine, organophosphates (pesticides or agents such as sarin), physostigmine, pyridostigmine Acetylcholine agonists: carbachol, choline, metacholine, pilocarpine

Sympathetic hyperactivity α and β-adrenergic activity

Agitation, mydriasis, Amphetamines, cocaine, sweating, flushing, pyrexia, ecstasy, ephedrine, tachycardia, hypertension PCP, phencyclidine, pseudoephedrine

If predominantly β-adrenergic

Tremor, tachycardia, hypotension

Caffeine, salbutamol, terbutaline, theophylline

If predominantly α-adrenergic

Bradycardia, hypertension

Phenylephrine, phenylpropanolamine

Extrapyramidal

Cog-wheel rigidity, tremor, trismus, hyper-reflexia, dyskinesia, dystonia, posturing, opisthotonos, choreoathetosis

Haloperidol, olanzapine, phenothiazines, risperidone

Hallucinogenic

Agitation, psychosis, hallucinations, mydriasis, hyperthermia

Amphetamines, cannabinoids, cocaine, LSD

Narcotic

Decreased consciousness, miosis, bradypnoea, bradycardia, hypotension, hypothermia, bowel stasis

Clonidine, dextromethorphan, opiates, pentazocine, propoxyphene

EMERGENCY MANAGEMENT

Table 14.5 (Continued) Toxidromes

Constellation of signs and symptoms

Possible toxins

Sedative

Confusion, slurred speech, dconsciousness, normal or reduced respiratory rate, normotension, normocardia

Anticonvulsants, antipsychotics, barbiturates, benzodiazepines, ethanol, GHB, meprobamate

Volatile inhalation

Euphoria, confusion, slurred speech, headache, restlessness, ataxia, seizures, respiratory depression, arrhythmias

Acetone, chlorinated hydrocarbons, fluorocarbons, hydrocarbons (petrol, butane, propane), nitrites (isobutyl, amyl, butyl), toluene

Serotonin

Agitation, confusion, Amphetamine, ecstasy, mydriasis, flushing, MAOIs, serotonin sweating, tremor, re-uptake inhibitors hyperreflexia, clonus, myoclonus, trismus, hyperthermia, tachypnoea, tachycardia, hypertension

Chemical pneumonitis

Cough, dyspnoea, wheeze, respiratory distress, cyanosis, fever Can occur without aspiration or loss of consciousness

Essential oils, petroleum distillates, turpentine, white spirit

Methaemaglobinaemia

Headache, diminished consciousness, dyspnoea, tachypnoea, severe hypoxia, tachycardia, chocolate coloured blood

Alanine dyes, benzocaine, chlorates, chloroquine, dapsone, nitrates and nitrites, nitrobenzene, nitrophenol, phenacetin, phenazopyridine, primaquine, sodium nitroprusside

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Immediate management Rapid simultaneous assessment of the patient, and of the likely agent(s) involved, may aid management. Details of which agent(s), how much, and how long ago should be actively sought; the following may help: • History from patient, family, other witnesses, or paramedics. • History of repeat prescriptions from GP. • Examination of patient for signs associated with certain drugs. • Examination of pill bottles or tablets; a pill identification system such as the computer-aided tablet and capsule identification program (TICTAC) may be required. Resuscitation • Give O2 and support airway, breathing, and circulation as required. Airway support • Endotracheal intubation may be required if the following is present: • Hypoxia • Diminished consciousnes (GCS 9, or rapidly deteriorating) • The patient is at risk of aspiration • The patient is agitated, or combative and not mentally competent • Any corrosive substances have been ingested Breathing support • Ensure ventilation is adequate, use mechanical ventilation if necessary: • Respiratory stimulants are unhelpful • In conditions where there is extreme acidosis it may be appropriate to hyperventilate the patient for a short period Circulatory support • Fluid loading may be required to treat hypotension: • Tachypnoea, sweating, and prolonged unconsciousness can lead to fluid depletion • Inotropes are occasionally required, but may interact with overdoses of cardiovascular drugs; where there is doubt discuss their use with an expert in poisonings • Hypotension may be the result of arrhythmias requiring treatment; treat any cardiac arrhythmias and conduction defects which may compromise the circulation (see b p.132 and 138). • Correction of hypoxia, acidosis (both metabolic and respiratory), and electrolytes will be required • Where tricyclic antidepressants are involved a bolus of 50–100 ml sodium bicarbonate 8.4% IV may help • Where drugs have prolonged the QT interval resulting in torsade de pointes, it may be treated with magnesium sulphate 8 mmol (2 g) in 100 ml 5% glucose IV over 2–5 minutes followed by an infusion of 2–4 mmol/hour (0.5–1 g/hour) (10 mmol) and potassium supplementation (40 mmol in 100 ml 5% dextrose over 1–4 hours via a central line aiming for a plasma concentration of 4.5–5.0 mmol/L)

EMERGENCY MANAGEMENT

• Profound bradycardia may be caused by certain agents, and may be unresponsive to drug therapy, requiring: • Early transvenous or transcutaneous pacing • Chemical pacing with adrenaline or isoprenaline • β-blocker toxicity may require treatment with glucagon 2–10 mg IV/IM, and calcium channel antagonist toxicity may require calcium chloride 10 ml 10% IV; additional treatment for bradycardia and/or hypotension may also be necessary (see b pp.104 and 132) • In digoxin overdose treatment with Fab fragments may help • Hypertension can occur with some drugs, particularly amphetamines and cocaine– hypotensive agents may be required. Neurological support • Convulsions are mostly brief and non-sustained; where status epilepticus occurs first-line treatment is with a short-acting benzodiazepine such as lorazepam 4 mg IV (see b p.160): • Be aware that many patients will have taken benzodiazepines as part of their overdose ‘cocktail’ • Dystonic reactions can occur and may require treatment with procyclidine 5–10 mg IV. Prevention of absorption Activated charcoal • 50–100 g PO of activated charcoal can be used if patients have ingested a potentially toxic dose of a poison within the past 1 hour: • Activated charcoal is contraindicated in patients at risk of aspiration, e.g. patients with dconsciousness or after hydrocarbon ingestion; it is also relatively contraindicated in patients at risk of GI bleeding or perforation • In patients with diminished consciousness, charcoal can be safely delivered via a NGT if the airway is protected by cuffed ETT and the NGT position has been positively confirmed • It is ineffective against alcohols, solvents, metal salts (e.g. iron and lithium), petroleum distillates, DDT, and malathion • Do not give alongside an oral antidote • Multiple-dose activated charcoal may be used for certain drugs, (phenobarbital, carbamazepine, dapsone, quinine, and theophylline) at a rate not less than 12.5 g/hour. Gastric lavage • Gastric lavage is not routinely recommended. It should only ever be considered in case of extreme risk from recent ingestion (1 hour prior to admission, or where the timing of ingestion is unknown; where there is doubt discuss the case with a poisons expert. • ‘Body-packers’ (drug couriers who have ingested packages filled with drugs), require a surgical referral, treatment will depend upon the risks posed by the drug(s) involved and their position within the GI tract. • Self-poisoning requires appropriate evaluation of any future suicide risk; ideally this should be arranged prior to ICU discharge.

Legal pitfalls • Deaths from poisoning should be reported to the coroner. • Most patients will cooperate with treatment though some, particularly those who have attempted suicide, may refuse it: • Patients who are mentally competent have the right to refuse any, and all, treatment, even if they risk death in doing so • Mental competency requires the ability to understand, retain, believe and evaluate information • Life-saving treatments may be administered to patients against their will only if they are not mentally competent and have no legally binding advance directive. • When in doubt ask for senior advice or psychiatric advice early. • Carefully document any refusal of treatment, or any treatment against a patient’s wishes.

Further reading Brooks DE, et al. Toxicology in the ICU. Part 2: Specific toxins. Chest 2011; 140(4): 1072–85. Joint Formulary Committee. Emergency treatment of poisoning In British national formulary. London: BMJ Group and Pharmaceutical Press, latest edn September 2012. Position paper on urine alkalinization. Clin Toxicol 2004; 42(1): 1–26. Position paper: gastric lavage. Clin Toxicol 2004; 42(7): 933–43. Position paper: whole bowel irrigation. Clin Toxicol 2004; 42(6): 843–54. Position paper: single-dose activated charcoal. Clinical Toxicol 2005; 43: 61–87. Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. Clin Toxicol 1999; 37(6): 731–51. Mental Capacity Act 2005. London: HMSO, 2005. Levine M, et al. Toxicology in the ICU. Part 1: general overview and approach to treatment. Chest 2011; 140(3): 795–80. Levine M, et al. Toxicology in the ICU. Part 3: natural toxins. Chest 2011; 140(5): 1357–70. TICTAC tablet identification system: M . TOXBASE—web-based database of the National Poisons Information Service available to registered users (i.e. A&E departments): M .

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Analgesics ! Paracetamol poisoning Paracetamol (acetaminophen) is a common hepatotoxic agent in deliberate overdose. It is found in many over-the-counter medications. Causes • Paracetamol poisoning occurs when healthy individuals take moderate to large overdoses (10 g/20 tablets or 150 mg/kg within 24 hours). • Certain patients have depleted stores of glutathione and are susceptible to hepatotoxicity at much lower doses, including: • Malnourished: anorexia, alcoholism, HIV • Taking enzyme inducing drugs: carbamazepine, phenobarbital, phenytoin, primidone, rifampicin, St John’s wort • In rare cases in high-risk individuals, poisoning may occur at normal doses administered over a prolonged time. Presentation and assessment • Initial presentation is mostly asymptomatic unless other agents are also involved, although nausea and vomiting may occur. • In exceptionally high overdoses (>5000 μmol/L or 800 mg/L) acute deterioration in GCS may occur accompanied by lactic acidosis. • Delayed presentation (12 hours–4 days) can be accompanied by RUQ pain with liver and/or renal failure. • Liver damage is maximal at 4 days after the overdose, and may result in encephalopathy, cerebral oedema, haemorrhage, and hypoglycaemia. Investigations (See also b p.449.) • ABGs, if compromised (acidaemia). • FBC and coagulation studies (deranged INR). • U&Es, LFTs (raised transaminases). • Serum glucose (hypoglycaemia may occur). • Serum paracetamol levels (at 4 hours post ingestion if possible).

Immediate management (See also b p.454.) • Give O2 and support airway, breathing, and circulation as required. • Treatment is guided by plasma levels taken >4 hours after ingestion, levels (earlier levels are misleading); high-risk patients require treatment at lower plasma levels (see Fig. 14.1). • If history is suggestive of an overdose in the past 36 hours requiring treatment then commence IV N-acetylcysteine whilst awaiting levels. • Methionine can be given if poisoning is 12 hours after ingestion may be misleading low • Acidaemia, or severe symptoms, also indicate high levels

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• Levels >500 mg/L (3.6 mmol/L) are an indication for urinary alkalinization by giving 200–300 ml IV boluses of 8.4% sodium bicarbonate: • Bicarbonate may also be used to correct metabolic acidosis • Levels >700 mg/L (5.1 mmol/L) are an indication for haemodialysis. • Checked and replace potassium levels alongside urinary alkalinization. • Serial blood glucose measurement (and correction) is required. • Sedatives, or induction of anaesthesia, may decrease ventilation, and worsen acidaemia (encouraging further salicylate movement into the brain) prophylactic bicarbonate should be given in these situations. Further management (See also b p.456.) • FBC and U&E monitoring are advisable after large NSAID overdoses. • Serial measurements of ABGs and U&Es will allow the monitoring of salicylate overdose progression. • A salicylate level 100 msec (associated with i arrhythmia incidence) • Other: hyperthermia, metabolic acidosis, hypokalaemia. Investigations (See also b p.449.) Plasma levels do not aid management; qualitative drug screens may be affected by other drugs (e.g. carbamazepine and diphenhydramine) • Core temperature • ABGs (respiratory and/or metabolic acidosis) • FBC, U&Es (hyperkalaemia, or hyponatraemia), LFTs • Serum CK (rhabdomyolysis may occur) • Serum glucose (exclude hypoglycaemia) • 12-lead ECG (see above) • Consider head CT scan to exclude other causes of unconsciousness. Differential diagnoses The combination of neurological and cardiac signs and symptoms are found in other illnesses including: intracranial haemorrhage/subarachnoid haemorrhage, meningitis/encephalitis, and sepsis.

ANTIDEPRESSANTS

Immediate management (See also b p.454.) • Give O2 and support airway, breathing, and circulation as required. • ECG monitoring is essential. • Markers of severe toxicity include: dconsciousness or seizures, cardiac arrhythmias/conduction defects, hypotension, respiratory depression, QRS prolongation. • If ingestion 25% the possibility of late-onset neurological complications may be lessened by hyperbaric oxygen • Other indications include COHb >40%, episode of unconsciousness, neurological disturbance, ECG changes, and pregnancy • Cerebral oedema may require treatment with mannitol. Pitfalls/difficult situations • Inhaled gases from fires may cause other complications, including cyanide/cyanate poisoning or inhalational injury.

4 Cyanide Cyanide poisoning is associated with smoke inhalation injuries and with industrial accidents, as with CO a high index of suspicion is required. Signs and symptoms may include headache, convulsions, coma, tachypnoea cardiac ischaemia, arrhythmias, pulmonary oedema metabolic acidosis, and cardiac arrest. Investigations (See also b p.449.) • FBC, coagulation studies, U&Es, LFTs, ABGs, and ECG are all required. • Blood should be taken for cyanide levels, but treatment should not be delayed if there is a clear history of exposure.

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Immediate management (See also b p.454.) • Patients should be decontaminated prior to examination/treatment • Support airway, breathing, and circulation as required • High concentration O2 is required: • Inhaled amyl nitrite may provide a rapid temporary treatment • Consider IV sodium nitrite (10 ml of 3% over 3 minutes) followed by sodium thiosulphate (25ml of 50% over 10 minutes) • Dicobalt edetate is toxic and reserved for confirmed severe cases.

Further reading Ilano AL, et al. Management of carbon monoxide poisoning. Chest 1990; 97: 165–9.

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Industrial chemicals 4 Organophosphates and carbamates Industrial exposure and deliberate self-poisonings with organophosphates and carbamates are common, particularly in the developing world. Causes Organophosphates such as malathion, parathion, dichlorvos and phosmet are agricultural insecticides (malathion is also used for the treatment of body/head lice). Carbamates are also insecticides or insect repellents. Organophosphates/carbamates inhibit acetylcholinesterase, allowing acetylcholine to accumulate/trigger autonomic and skeletal receptors. Carbamate poisoning is generally less severe and of shorter duration. Chemical nerve agents (e.g. G-agents such as sarin, tabun and soman; V-agents such as VX gas) are similar to organophosphates, and require similar treatment (see also b p.496). Presentation and assessment These agents can act via ingestion, inhalation or transdermally. A classic ‘toxidrome’ of cholinergic effects may be seen (b p.452) including: • Excess salivation/secretions, sweating, miosis, and blurred vision. • Vomiting, diarrhoea, abdominal cramps, faecal/urinary incontinence. • Headaches, dizziness, tremors, ataxia, dystonia, seizures, coma. • Muscle weakness, fasciculations, and paralysis (all occur late). • Bradycardia, hypotension. • Bronchorrhoea, bronchospasm, respiratory depression. Investigations (See also b p.449.) • RBC cholinesterase activity can be measured in suspected poisoning. • ABG (hypoxia, hypercapnia). • FBC, U&Es, LFTs. • Serum glucose (hypoglycaemia or hyperglycaemia may occur). • ECG (ST changes, peaked Ts, AV block, prolonged QT, arrhythmias). • CXR (diffuse opacities, pulmonary oedema).

Immediate management (See also b p.454.) • Patients should be decontaminated prior to examination/treatment. • Give O2 and support airway, breathing, and circulation as required. • Intubation/ventilation may be required if there is respiratory distress. • Atropine 2 mg IV should be given every 20 minutes until pupils dilate, skin is dry, and tachycardia occurs. • In moderate to severe cases pralidoxime can be given (within 24 hours), 30 mg/kg IV with 1 to 2 further doses as required. • Benzodiazepines may control agitation or seizures (b p.160).

Further management (See also b p.456.) • Paralysis requiring ventilation may occur days after ingestion. • Repeated pralidoxime doses may be required until atropine is no longer needed.

INDUSTRIAL CHEMICALS

4 Phenoxyacetates Phenoxyacetate pesticide poisoning signs and symptoms include: • Neurological: diminished consciousness, seizures. • Neuromuscular: myotonia, myositis, weakness, fasciculation. • GI: burning mouth/throat, nausea, vomiting, diarrhoea. • Other: sweating, hypertension, hyperthermia, rhabdomyolysis. Investigations (See also b p.449.) • ABGs (metabolic acidosis is common). • U&Es and serum calcium (hypocalcaemia is common). • Serum glucose (hypoglycaemia is common). • Serum CK, urine myoglobin will be required (rhabdomyolysis). Immediate management (See also b p.454.) • Patients should be decontaminated prior to examination/treatment. • Give O2 and support airway, breathing, and circulation as required: • Neuromuscular weakness may require mechanical ventilation • 2,4 dichlorophenoxyactic acid and meoprop may be treated with forced alkaline diuresis. • Other phenoxyacetates may be treated by haemodialysis.

3 Paraquat Paraquat poisoning initially presents as the ingestion of a corrosive agent. Cardiovascular collapse, pulmonary oedema, and metabolic acidosis may occur. Urine testing confirms the diagnosis, and plasma concentrations give prognostic information. Initial treatment is with oral/NG Fuller’s earth. High O2 concentrations may worsen pulmonary toxicity. Later complications include liver or renal failure, but a progressive alveolitis over a few days is the most common cause of death.

4 Strychnine Strychnine poisoning causes intense muscle spasms that may resemble tonic/clonic epilepsy (though the patient should be awake) or tetanus. Respiratory distress may occur, requiring endotracheal intubation and mechanical ventilation with neuromuscular blockade. U&Es and CK should be measured as rhabdomyolysis, renal failure, and hyperthermia may occur, requiring supportive treatment.

4 Chlorine Chlorine exposure can cause haemoptysis, dyspnoea, bronchospasm, and pulmonary oedema. Toxicity can occur up to 24 hours after exposure, but is unlikely if the eyes have been exposed but are asymptomatic. Laryngeal damage will necessitate early endotracheal intubation (see b p.30). Bronchodilators may help alleviate respiratory distress, but mechanical ventilation is likely to be required in severe cases.

Further reading Eddlestome M, et al. Management of acute organophosphate poisoning. Lancet 2008; 371: 597–607.

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Alcohols and hydrocarbons 3 Ethylene glycol and methanol Ethylene glycol and methanol are both found in antifreeze solutions; methanol is found in household products and illegally produced spirits. Presentation and assessment • Intoxication, nystagmus/ataxia, seizures, dconsciousness. • Nausea, vomiting, flank (ethylene glycol) or abdominal pain (methanol). • Tachycardia, hypotension, cardiogenic shock. • Metabolic acidosis, tachypnoea, and respiratory distress. • Methanol may produce marked visual disturbances. • Ethylene glycol causes pulmonary oedema and renal failure. Investigations (See also b p.449.) • Serum methanol and ethylene glycol levels to confirm the diagnosis. • ABGs and serum osmolality (methanol and ethylene glycol cause a very pronounced metabolic acidosis with a raised anion gap, >12 mmol/L, and raised osmolar gap, >10 mOsm). • Serum U&Es (renal failure in ethylene glycol poisoning). • Serum calcium, phosphate and magnesium (all d with ethylene glycol). • Serum glucose (hyperglycaemia occurs with methanol poisoning). • Urine microscopy (oxalate crystals in ethylene glycol poisoning). • CXR (infiltrates, pulmonary oedema). Differential diagnoses • Conditions causing altered consciousness/behaviour, or metabolic acidosis (e.g. alcohol intoxication, head injuries, sepsis).

Immediate management (See also b p.454.) • Give O2 and support airway, breathing, and circulation as required. • Charcoal is ineffective, gastric lavage may be appropriate (b p.455). • Ethanol should be given orally (loading dose 1 ml/kg 50%, 750g or 1 cup of spirits), or IV (loading dose 7.5 ml/kg 10% over 30 minutes): • Serial serum ethanol levels will be needed (aiming for 0.8 g/L) • Alternatively IV fomepizole may be used, if available (loading dose 15 mg/kg over 30 minutes, followed by 10 mg/kg 12-hourly). • Folinic acid 30 mg IV 6-hourly should be given in methanol poisoning • IV sodium bicarbonate may be required to treat acidosis. • Haemodialysis should be commenced if ethylene glycol level is >500 mg/L, or acidaemia (pH 1 mcg/kg/ hour, titrated to effect) Further management (See also b p.456.) • Trauma and compartment syndrome are associated with opioids. • Unusual infections such as tetanus and botulism are associated with illicit IV or IM drug usage, as are HIV, HBV and HCV; appropriate precautions should be taken.

RECREATIONAL DRUGS

Pitfalls/difficult situations • Paracetamol co-drugs contain opioids including codeine and dextropropoxyphene (co-proxamol, available but no longer licensed). Dextropropoxyphene has long-acting opioid effects and has a cardiotoxic metabolite, the treatment of which may require magnesium and/or bicarbonate.

3 Cocaine Severe poisoning with cocaine may cause: • Severe hypertension, vasoconstriction, and hyperthermia. • Hyper-reflexia, convulsions, coma, intracranial bleeds or infarcts. • Myocardial ischaemia, arrhythmias, cardiogenic shock, cardiac arrest. • Rhabdomyolysis and renal failure. Investigations should include core temperature, U&Es, serum CK, cardiac troponins, 12-lead ECG, and possibly echocardiography or angiography. Immediate management (See also b p.454.) • Give O2 and support airway, breathing, and circulation as required. • ECG monitoring is essential. • Treat hypertension or cardiac ischaemia initially with benzodiazepines, α-blockers or IV nitrates: • Ischaemic crises should be treated with aspirin • Obtain cardiology advice in patients chest pain/ischaemia • β-blockers may worsen hypertension • Hyperthermia should be treated by cooling and other treatments, including dantrolene if required (see b p.248).

3 Amphetamines and ecstasy Amphetamines and MDMA (ecstasy) can cause agitation, convulsions, and coma. Arrhythmias are common, as is hypertension. Patients are often dehydrated, although in some patients excessive water consumption leads to a hypo-osmolar state. Investigations should include FBC, coagulation studies, U&Es, LFTs, serum CK, serum glucose, and ECG. Hypertension caused by amphetamines or ecstasy should be treated in the same way as hypertension caused by cocaine. An idiosyncratic hyperthermic reaction can occur and is associated with muscle rigidity, rhabdomyolysis, metabolic acidosis, renal failure, hepatic failure, convulsions, coma, and DIC. Cooling and other treatments for hyperthermia may be required (see b p.248) along with dantrolene.

3 Ketamine and LSD Ketamine is sedative in nature. Airway support and, in severe poisoning, treatment for convulsions and raised ICP may be required. Emergence delirium/agitation may occur requiring treatment with benzodiazepines.

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LSD is relatively benign. Hallucinations may lead to marked agitation or bizarre behaviour. Coma, convulsions, bleeding, and pyrexia sometimes occur. Sedation may be required with benzodiazepines.

3 Cannabis Cannabis is relatively safe except when injected. IV cannabis can cause hypotension, pulmonary oedema, DIC, and renal failure.

Further reading Devlin RJ, et al. Clinical review: major consequences of illicit drug consumption. Crit Care 2008; 12: 202.

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Miscellaneous poisons 3 β-blockers and calcium channel antagonists

β-blockers and calcium channel antagonists are commonly prescribed in patients with cardiac conditions, which are likely to exacerbate the effects of inadvertent or deliberate overdose. Presentation and assessment Common signs and symptoms of β-blocker overdose include: • Dizziness, syncope, bradycardia, complete heart block. • Ventricular arrhythmias, torsade de pointes (particularly with sotalol). • Hypotension, heart failure. • Respiratory depression, bradypnoea, bronchoconstriction. • Coma, seizures (particularly with propranolol). • Hypoglycaemia, rhabdomyolysis, AKI, metabolic acidosis. Signs and symptoms of calcium channel antagonist overdose include: • Nausea, vomiting, hypotension, vasodilatation. • Dizziness, agitation, confusion, coma. • QT prolongation, bradycardia, complete heart block, asystole (verapamil, diltiazem). • Respiratory distress, ARDS, metabolic acidosis, hyperglycaemia. Investigations (See also b p.449.) • ABG (metabolic acidosis, hypoxia, hypercapnia). • Serum glucose (hypoglycaemia or hyperglycaemia), serum CK. • ECG (bradycardia, AV block, prolonged QT, arrhythmias). • CXR (ARDS). • Consider head CT scan to exclude other causes of unconsciousness. Differential diagnoses • Conditions causing hypotension and bradycardia (e.g. cardiac disease). Immediate management (See also b p.454.) • Give O2 and support airway, breathing, and circulation as required. • ECG monitoring is essential. • If ingestion 2.5 mmol/L is associated with toxicity • U&Es (to monitor for renal failure and hypernatraemia). • Serum Ca2+ (to monitor for hypercalcaemia). • 12-lead ECG (conduction abnormalities or ST/T wave changes). Immediate management (See also b p.454.) • Give O2 and support airway, breathing, and circulation as required. • Charcoal does not work, but gastric lavage may be of benefit (if appropriate). • ECG monitoring is recommended. • Volume replacement with isotonic saline fluids may be required • Haemodialysis should be considered if: • Levels >7.5 mmol/L for acute overdoses in patients who are lithium naıï ve, or • Levels >2.5 mmol/L in patients on chronic treatment, or • In acute-on-chronic OD, or • Where symptoms are severe • Haemofiltration may be used, but is less effective and will take longer to lower levels.

1 Lead The acute presentation of lead poisoning is an encephalopathy with ataxia, convulsions, and coma; associated with abdominal pain and vomiting. A peripheral motor neuropathy (foot and wrist drop) may occur. Investigations (See also b p.449.) • Blood lead levels can be estimated. • FBC (anaemia with basophilic stippling, and RBC fluorescence). • U&Es (reveal renal dysfunction).

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Immediate management (See also b p.454.) • Give O2 and support airway, breathing, and circulation as required. • Charcoal does not work. • Chelation therapy with IV EDTA or oral DMSA (preferred) should be considered. Further management (See also b p.456.) • An ingested source should be looked for, as should any environmental contaminants.

3 Iron Iron poisoning usually occurs as a result of deliberate or accidental ingestion of large quantities of iron tablets. Presentation and assessment Iron initially acts as a GI irritant and may cause nausea and vomiting, abdominal pain, and GI bleeding. dconsciousness and convulsions may occur if overdose is severe, accompanied by hypotension, pulmonary oedema, and metabolic acidosis. Further complications may occur up to 48 hours after ingestion and can include: liver failure and/or renal failure, with accompanying metabolic acidosis, hypoglycaemia, and cardiovascular collapse. Investigations (See also b p.449.) • Serum iron levels should be taken at 4 hours post ingestion (or just prior to desferrioxamine if given at 90 μmol/L (5 mg/L) • Desferrioxamine causes hypotension • Whole bowel irrigation may be indicated for large overdoses.

MISCELLANEOUS POISONS

Further management (See also b p.456.) • Bowel ischaemia may occur requiring surgical treatment. • Pyloric stenosis causing gastric outlet obstruction is a late complication.

3 Corrosives, acids, alkalis, bleaches The main acute risk with these agents is airway or pharyngeal damage. If laryngeal oedema is present, early intubation should be considered even if the patient is currently asymptomatic. Early ENT or thoracic surgical involvement should be considered. Activated charcoal does not work and gastric lavage should not be attempted. Later complications include GI burns, which may require surgical intervention.

4 Local anaesthetic toxicity Local anaesthetic toxicity within critical care can occur if IV injection/infusion occurs (e.g. a local anaesthetic epidural infusion bag is mistaken for IV fluids), or if the soft-tissue dose given exceeds the maximum recommended dose.

Maximum recommended local anaesthetic doses • • • • •

Bupivacaine/levobupivacaine: Ropivacaine: Lidocaine: Lidocaine with adrenaline: Prilocaine:

2 mg/kg 3 mg/kg 3 mg/kg 6 mg/kg 6 mg/kg.

Presentation and assessment Signs and symptoms include: • Orofacial tingling/numbness, tinnitus, blurred vision, fasciculations. • dconsciousness, seizures, respiratory arrest. • Circulatory collapse with resistant arrhythmias.

Immediate management (See also b p.454.) • Stop giving the drug. • Give O2 and support airway, breathing, and circulation as required. • Endotracheal intubation and mechanical ventilation may be required. • Treat seizures as appropriate (b p.160). • Consider treating cardiovascular collapse/arrest with: ® • Intralipid 20% IV 1 ml/kg over 1 minute, repeated every 3–5 minutes to a maximum of 3 ml/kg

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3 Bites and stings Many snakebites are ‘dry’ (no injected venom), requiring no treatment, and many other bites or stings are of low toxicity. Expert advice is required to identify animals/insects and to direct treatment. Toxicity is generally either local (tissue necrosis) or systemic (cardiotoxic, neurotoxic, or coagulopathic, either via direct inhibition or consumption of clotting factors). Initially a compression lymph bandage may be applied (not a tourniquet) to slow the spread of any toxins. Antivenom may be advised for the treatment of certain snakebites, otherwise treatment is supportive. Bites, stings, and antivenom may cause anaphylaxis or anaphylactoid reactions (see b p.110).

Further reading Joint Formulary Committee. British national formulary, 64. London: BMJ Group and Pharmaceutical Press, September 2012. Odedra D, et al. Local anaesthetic toxicity. Curr Anaesth Crit Care 2010; 21: 52–4. Shepherd G. Treatment of poisoning caused by β-adrenergic and calcium-channel blockers. Am J Health Syst Pharm 2006; 63: 1828–35.

Chapter 15

Incidents and adverse events Suspected outbreaks 496 Major incidents 498 Adverse events, managing the aftermath 500

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3 Suspected outbreaks Suspected outbreaks may be associated with infections, biological agents, or poisonings (chemical, nutritional, or radioactive). Suspicious circumstances include: intelligence of a threat, multiple cases, simultaneous outbreaks elsewhere, and illness affecting a particular community.

Presentation and assessment • Illnesses which do not fit any recognizable clinical condition. • A known illness that is not expected in the setting where observed, or follows an unexpected course. Illnesses that should arouse suspicion include: • Clusters (>2) of patients with similar symptoms. • Signs and symptoms inappropriate to patient’s history/location. • Signs/symptoms of syndromes/toxidromes (see b p.452), such as: • Cholinergic activity: see b p.480 (G and V nerve agents) • Respiratory symptoms: chest tightness, pulmonary oedema, associated eye irritation (phosgene, chlorine, mustard gases) • Unexplained severe metabolic acidosis (cyanides) • Skin blistering, unexplained ‘thermal’ type burns • Fever with paralysis, mediastinal lymphadenopathy, or haemorrhagic thrombocytopaenia, see b pp.358 and 370 (anthrax, VHFs, tularaemia, pneumonic plague) • Aplastic anaemia, hair loss, severe GI loss

Investigations For biological agent exposure, the following samples may be requested: • Serum and whole blood EDTA (paired sample if recovery occurs). • Blood cultures (at least 1 sample prior to antibiotics if possible). • Sputum or bronchoalveolar lavage (if safe to do so). • Biopsy or aspiration samples of necrotic lesions or vesicles (vesicle swabs should be placed in viral transport medium). • Pus and/or swabs (take multiple samples). • Urine and other body fluids. • Stool or vomitus sample (if food contamination suspected). Take HPA advice on sample precautions. The specimen should be labelled with surname/forename/DOB, and transported to a clinical microbiology laboratory as soon as possible.

Further actions • Decontaminate before ICU admission; if unsure contact the HPA. • Make list of all staff who may have been exposed; treat waste, property and samples as hazardous until advised otherwise. • Use personal protective equipment as advised by HPA; if uncertain, use gloves, gown, cap, mask and eye protection (see b p.384 for instructions on how to don protective equipment in high-risk cases). • Give appropriate treatments where they are available: • Chemical poisoning: atropine and oximes, see b p.480 • Cyanide, see b p.458 • Anthrax/plague, see b p.358 • Tularaemia: doxycycline

SUSPECTED OUTBREAKS

• •

VHFs, see b p.370) Radiation: potassium iodide may be appropriate; in cases of internal exposure: chelation, ion exchange, or lavage may be possible

Further reading Health Protection Agency. CBRN incidents: clinical management and health protection. London: HPA, 2005. Health Protection Agency. Initial investigation and management of outbreaks and incidents of unusual illnesses: A guide for health professionals, 2010. Available at: M . White SM. Chemical and biological weapons. Implications for anaesthesia and intensive care. Br J Anaesth 2002; 89(2): 306–24. EMERGENCY CLINICAL SITUATION ALGORITHM IF ANY OF THE FOLLOWING UNUSUAL CLINICAL PRESENTATIONS OCCUR – CONSIDER DELIBERATE RELEASE • Unusually large numbers of patients present over a time period • Cases linked by epidemiological features • • • •

CBRN INCIDENTS hpa.org.uk/emergency/CBRN.htm

Similar features/ similar geographical area STEP 1-2-3 (see Box) Signs/ symptoms unusual or unusually severe Known cause but unusual in UK or where acquired Known cause but not responding to standard therapy Unknown aetiology

CBRN incidents: clinical managenet & health protection

Consider the risk of transmission or contamination to staff and/ or other patients *Isolate patient *Use standard personal protective equipment (PPE) - wear gloves, gown, and mask (add eye protection if patient coughing or vomiting) STEP 1-2-3

ACUTE

DELAYED

• over minutes to hours • occur in circumscribed geographical area • occur in people who may have shared a known

• over hours to days or days to weeks • may or may not occur in geographical clusters • may or may not occur in people who have

common exposure

Most likely: CHEMICAL Other possibilities: Biological toxins Radiological

shared a known common exposure • detected by surveillance

Most likely: INFECTIOUS AGENT Other possibilities: Radiological Psychological Chemicals (latent period)

The following precautions should be taken before continuing with the assessment. First Actions One Casualty Treat as normal Two Casualties Have a low index of suspicion but otherwise treat as normal Three Casualties or More Initial assessment should be outside the department, use PPE, ask for SPECIALIST HELP

DECONTAMINATION

STAFF PROTECTION (PPE), HOSPITAL PROTECTION (air con, isolation) Initial clinical assessment, history and life saving management In the event of a chemical/ radiological incident, decontaminate the patient before admitting them to the department/ starting definitive treatment. Initiate local/ regional contingency plans.

1. Seek expert advice locally*

2. Ensure safety of self, other staff and patients

3. Detailed clinical assessment – use standard PPE (disposable gown, surgical mask, gloves, eye protection) • Nature and time course of symptoms • Detailed clinical history • Identify possible recent risk factors: o Where has the patient been? o What has the patient been doing? o With whom/ what has the patient had contact?

4. Management as per best available advice • Take samples for laboratory investigations

5. Record information and communicate with • Senior clinician • Hospital management • Infection control • Local medical microbiologist & chemical pathologist • Laboratories • Local HPU • Chemical hazards and Poisons Division (of the HPA) • Local Radiation Protection Advisor HPA Emergency Clinical Situation Algorithm V1 (24 August 2006)

Rinse-Wipe-Rinse Step 1 Gently wash affected areas with soapy water (0.9% saline for open wounds and eyes): this dilutes the contaminant and removes particles and water based chemicals Step 2 Wipe affected areas gently but thoroughly with sponge or soft brush or washcloth: this removes organic chemicals and petrochemicals Step 3 Gently rinse affected areas *Inform local HPU IMMEDIATELY http://www.hpa.org.uk/lar s_hpus.htm HPU to contact HPA CfI IMMEDIATELY 24hr Tel: 020 8200 4400 or 6868 In Northern Ireland inform CCDC CCDC to inform CDSCNI Tel: 028 7926 3755 Inform hospital infection control Inform local laboratory of sample status

Fig. 15.1 Algorithm for the management of outbreaks. Reproduced with permission from the Health Protection Agency.

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2 Major incidents A major incident may be external (a disaster in the community) or internal (e.g. a fire). It is loosely defined as any incident that generates sufficient numbers/types of casualties as to require special arrangements. Every hospital (and ICU) should have a major incident plan of which staff should be aware. A major incident should trigger involvement of senior management within the hospital to co-ordinate an effective response from different clinical departments. ICU staff may have to work closely with operating theatres, A&E, and other high dependency areas within the same hospital and/or other hospitals. The hospital major incident plan will detail the command and control structure (both sites and personnel). This will include which individuals have responsibility for different areas/roles, including ‘on scene’, A&E, triage, theatres, and communications. The p role of intensive care physicians is usually to manage ICU patients whilst simultaneously expanding critical care capacity.

Major incidents and ICU Consider suspending elective admissions for the duration of the incident.

Management All areas of the hospital should have ‘action cards’ available, designating major incident roles and chain-of-command; and detailing emergency telephone numbers. Senior ICU staff should take over management/coordinating roles. They should ensure that the following are in place: • Effective triage system required for appropriate allocation of resources. • Assessment of the likely burden and its impact on existing services. • Assessment of risk to other patients and staff; strategies for risk containment. • Identification of extra capacity. • Coordination with other clinical departments and hospital management.

Staff • Activate a direct-line phone for all communications with staff; avoid using hospital switchboard. • Call extra staff as required: • Be prepared to identify and call non-ICU staff who may also provide help (e.g. recovery nurses, theatre staff) • Staff should not come in unless they are contacted • Do not call in all staff; retain reasonable numbers for second, third, and subsequent shift changes: • Keep original shift patterns if possible • All members of staff should have clearly defined roles within the team. • All staff should carry their hospital ID cards with them at all times.

MAJOR INCIDENTS

Identifying extra capacity ICUs should have ‘surge’ plans that can be activated in the event of a sudden increase in demand for ICU beds. Actions include: • Identify patients who may be safely discharged from critical care. • Identify patients who may be safely transferred to other units. • Identify capacity in nearby hospitals and keep them on alert. • Identify other areas where extra patients can be managed (e.g. theatres, recovery). • Identify and check equipment which can be used (e.g. syringe drivers, theatre ventilators).

Allocating roles • Where possible, task-specific roles may be allocated (i.e. 1 member of staff preparing all IV infusions). • Use flexible dependency systems (i.e. 1 critical care trained nurse to 2 level three patients). • Where possible cohort patients with similar pathology to be cared for by 1 team. • Allocate staff to transfer teams if required.

Communication • The hospital internal telephone system may become overrun; a runner should be allocated to ICU. • Keep families informed as much as possible, but only where face-toface communication is possible; do not give out details over the phone. • Do not communicate directly with the press, direct them to appropriate designated personnel (communication officer). • Keep all channels of communication open. • Arrange regular updates with other clinical departments (A&E, theatres) and senior hospital management.

Intensive care triage In times of extreme pressure on resources it may become necessary to actively triage patients in order to maximize the delivery of healthcare to those patients most likely to benefit. Various systems of triage exist, but most attempt to categorize patients into 3 broad groups: those with critical illness who are unlikely to survive; those who are not critically ill, and for whom definitive treatment can be safely delayed; those who are critically ill, but are deemed salvageable (the group to whom resources are preferentially allocated).

Further reading Mahoney EJ, et al. Mass-casualty incidents: how does an ICU prepare? J Intensive Care Med 2008; 23: 219–35.

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3 Adverse events, managing the aftermath Adverse events may lead to severe patient harm or death. Such a catastrophe has a major impact on patients, relatives, and staff. Providing appropriate care to the patient, and practical help and support to the relatives and the staff, are part of good clinical governance and risk management.

Immediate actions • Consult departmental/hospital guidelines on the actions required in the event of an adverse incident. • Accurate and contemporaneous records are vital: • A full retrospective account must be recorded as soon as possible • Records should be legible, timed, dated, and signed • Where possible, electronic copies of monitoring be printed and filed • Original charts and notes must not be altered in any way; amendments, if any, must be recorded separately • If possible, make personal notes for reference at a later date Dealing with the patient • In cases where death has resulted, leave all lines, tubes, and equipment in place, and inform the coroner. • In case where the patient survives, consider asking a colleague to help and take over their care. Dealing with relatives • Do not break bad news over the telephone if at all possible; invite the relatives to come to the hospital; inform them that some complication had occurred, but provide no further details. • Be polite with them all the time; if possible get a senior colleague or member of the team to help deal with relatives. • Any interview with relatives should be a team approach; other members of the team could be surgeons, physicians, nurses, and colleagues. • Offer a full explanation of any events, as far as they are known: • Avoid ‘underplaying’ the severity or seriousness of events • If the facts are not clear, avoid speculation (e.g. as to the cause of any event, or regarding any events which may have occurred before your involvement) • Inform relatives that a full investigation will take place, and that this may take some time. • Further interviews may be necessary. • In cases where death has occurred, involve the hospital bereavement services. Dealing with staff • A senior colleague should attend the hospital and help in dealing with the aftermath.

ADVERSE EVENTS, MANAGING THE AFTERMATH

• A decision will need to be made as to whether the members of staff involved are in a reasonable condition to continue with their duties. • The clinical director should be involved at an early stage. • The staff involved should contact their medical protection organizations at the earliest possible opportunity. • Staff should cooperate with investigation, and not isolate themselves.

‘Later’ actions Communications • The clinical director, or a consultant not involved with the incident, should talk to senior hospital management, if necessary. • The incident should be reported to local and national incident reporting channels. • The communications officer, and complaints manager, within the hospital will require briefing of the adverse event. Equipment and drugs • The clinical director, or a consultant not involved with the incident, should check the patient, drugs, equipment, and records. • Any faulty equipment should be de-commissioned. • All pieces of equipment, records, imaging, and drug ampoules should be stored in a secure place for further investigation, if required. • An accurate record of any equipment/drug checks should be maintained. The ICU team • A debriefing should be organized with the team to provide information and gain feedback. • Any anxieties and misconceptions should be allowed to be aired, and then dealt with appropriately. • The services of a trained counsellor may be required to assist staff. The media • Media enquiries, if they arise, should be directed to the communications officer within the hospital. The role of the department • Colleagues should allow the member of staff involved in the incident, to ‘talk about it’, without being judgemental. • A group of colleagues may be required to lead a root cause analysis of the event. • A senior colleague may be informally assigned to provide mentorship and support to the staff involved in the incident. • Individuals involved are likely to need further support, e.g. from occupational health: • Where staff are severely affected by the event, they may suffer daydreams, flashbacks, restlessness, apathy, anger, fear, guilt, relationship problems, alcohol dependence and physical manifestations of stress

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Possible outcomes (depending on the severity of the event and the circumstances involved) • Local route cause analysis, including presentation of ‘lessons learnt’ in a meeting. • Suspension of the staff involved in the incident, pending investigation. • Involvement of deaneries and royal colleges in the case of trainees. • Disciplinary actions by the General Medical Council or other regulatory body, which may involve retraining, and/or further assessment. • Criminal prosecution or civil litigation.

Reporting an incident In the majority of critical incidents, individual error is only a small fraction of the problem. The main problems are the latent factors inherent in unsafe systems (i.e. faulty design, poor resources, poor communication) which create conditions in which a simple mistake leads to the incident. A system of reporting critical incidents, and learning from them, is central to patient safety and clinical governance within a hospital. All hospital staff should report any critical incident, at least at local level, in which they may have been involved. Incident reporting in ICU Each ICU should have robust incident reporting systems and a clinical governance lead. Ideally this system should also feed in to the hospital systems and/or national systems. All staff should be aware of the system, how to access it, what to report and then what to expect. Periodic meetings, case discussions, root cause analysis, and initiatives to improve systems will be required to keep all staff engaged. Systems should also be in place to support the patient, relatives, and staff involved in the incident. Core principles of an incident reporting system • The main aim is to learn from incidents, so that systems can be improved to prevent incidents from recurring. • In order to encourage staff to report, the system should be based on a non-punitive approach; i.e. rather than looking at ‘who’ was involved in the incident, we should be looking at ‘how’ the incident was caused and ‘what’ system improvements can be made to prevent it from recurring in future. • It should allow free text so that staff can narrate what actually happened, with very few, if any, closed questions. • If the reporter so desires, it should allow anonymity. • The reporter should be able to submit it anytime, although early submission should be encouraged. • It should be easy for the staff to report without worries of any punitive action. • It should not take more than few minutes to report a typical incident.

ADVERSE EVENTS, MANAGING THE AFTERMATH

• All incidents should be analysed, exploring institutional, organizational, environmental, team, individual, and patient factors: • Analysis should define the problem and suggest solutions • Analysis of incidents should be fed back using multiple channels (e.g. newsletters, e-mails, networking, safety meetings)

Training for emergencies (human factors) Individuals are more likely to make mistakes when the demand on their cognition exceeds their capacity to handle (i.e. during emergency situations in a busy ICU). Systems should be in place whereby the chances of mistakes made by an individual member of the team are minimized (e.g. checklists, team working, protocols, alerts).Training for emergencies for ICU staff should have 2 components: • Technical skills • Non-technical skills Training in non-technical skills should have the following components: Situational awareness • Information gathering: structured handovers; good communication; visible monitoring and alarms. • Recognizing and understanding of the situation and its burden, resources, capacity, and priorities. • Anticipating likely changes. Decision-making • Identifying options. • Balancing risks and selecting options. • Seeking opinions of the team members. • Re-evaluating. Team working and leadership • Exchanging information. • Assessing capabilities and supporting other members of the team • Coordinating activities of the team members: • Confirm roles and responsibilities of individual team members • Discuss case with colleagues, and other specialists (e.g. radiologist, surgeon, microbiologist) • Consider requirements of others before acting • Focus on goals, and cooperate with others to achieve them Task management • Planning and preparing. • Prioritizing. • Maintaining standards. • Resource management. Training for emergencies: • Should have an educational lead in the unit. • Should ideally be undertaken in teams, involving all members of staff (e.g. physicians, nurses, managers).

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Utilize simulation centre facilities whenever possible. Practice case scenarios and major incidents on regular basis. Should incorporate de-briefing, reflection, and constructive feedback. Must incorporate training in non-technical skills. Evaluate non-technical skills of individual members of staff using standardized framework. • Should emphasize a systems-approach to errors. • Should incorporate strategies to improve systems to deal with emergencies (e.g. design, layout, resources, equipment, staff capacity and skill mix, channels of communication). • Should incorporate strategies to improve performance during an emergency (e.g. team approach, roles and responsibilities, nontechnical skills, leadership and priority, structured handovers/ communication, protocols, and checklists). • • • • •

Further reading Association of Anaesthetists of Great Britain and Ireland. Catastrophes in anaesthetic practice – dealing with the aftermath. London: AAGBI, 2005. Buckley TA, et al. Critical incident reporting in the intensive care unit. Anaesthesia 1997; 52: 403–9.

Chapter 16

Communication and organ donation Breaking bad news 506 Referral to the coroner 508 The potential organ donor 510

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3 Breaking bad news Communication with patients and their relatives should be part of ongoing care, and should, where possible, be provided at regular intervals or whenever the clinical situation changes. Given the severity of illness and high probability of death of patients requiring critical care, communicating bad news with patients and/or their families is a common occurrence. Breaking bad news can be difficult and distressing for all concerned. Where possible, the breaking of bad news should be led by a consultant who has received training in how to do this, but the speed with which patients deteriorate may mean that this is not possible, and what follows is a simplified template for ensuring that this is done as professionally as possible. It may need to be adapted for certain situations and according to the individuals involved.

Breaking bad news Preparation • Confirm you have the right patient and check the latest details regarding their condition and ongoing management. • Maintain relatives’/patient’s privacy if possible by using a quiet room or pulling curtains around bed. • Ensure you are not interrupted (if possible hand pagers and phones to someone else). • Where possible have the nurse caring for the patient present at the interview to ensure good continuity of information. • Introduce yourself to the patient or their relatives and confirm who you are talking with. • Sit at the same level as the person you are talking to and maintain appropriate eye-to-eye contact. What do the relatives or the patient know? • Enquire as to what information has already been passed on to the patient or their relatives. • Confirm their understanding of what they have already been told. What information is wanted? • Enquire as to what information they want to know next. Give a ‘warning shot’ • Give patients and relatives time to prepare for any bad news by giving a ‘warning shot’ such as: ‘I’m afraid I have some bad news’ or ‘I’m afraid the situation is very serious’. Allow relatives/patient to refuse further information • Some patients or relatives may not want to hear bad news at this point, and they should be allowed to refuse to hear any more at this time; if they refuse then inform them that they can always ask for more information in the future. • Relatives are not allowed to refuse on behalf of a relative who has capacity; it should be made clear that if the patient asks for information it will be given to them.

BREAKING BAD NEWS

Give explanation (if requested) • Give an honest explanation of the patient’s clinical condition and likely prognosis. • Use language which is clear and avoids, or simplifies, medical terms wherever possible. • Avoid euphemisms, where it is appropriate to use words such as ‘death’ or ‘dying’ then do so. • Do not provide false reassurance. • If you do not know the diagnosis or likelihood of injury/death then it is appropriate to say so, it is also appropriate to explain in terms of what you suspect the most likely diagnosis/outcome will be. • Re-iterate important points and confirm that they are understood: ‘Does that make sense?’ Listen to concerns • Enquire as to whether the patient/relatives have questions they want to ask. Time must be provided for them to absorb information and to ask questions—their agenda may be very different from what you are expecting and it is important to listen to any concerns. Encourage expression of feelings • A phrase such as ‘How does that news leave you feeling?’ may allow the relatives or patient to express their feelings and emotions which may be therapeutic in its own right. Summarize explanation and explain plan, then offer availability and support • Ensure that the patient or their relatives are aware that you, or a member of your team, will be available to provide further information as and when it is requested. Communicate with team • A summary of the conversation should be recorded in the patient’s medical records; this should include any key points along with any specific concerns raised. Adapted from Guidelines for communicating bad news with patients and their families, East Midlands Cancer Network (2010) by P Costello and G Finn, with permission M http://www. eastmidlandscancernetwork.nhs.uk/Library/BreakingBadNewsGuidelines.pdf

Pitfalls/difficult situations • Communication is a process. The severity of a situation may require several conversations with different clinicians before it is fully accepted. • Patients/relatives may be angry about the situation or about previous management. This anger should be acknowledged, and where appropriate an apology offered. Do not enter into criticism of previous management.

Further reading Buckman R. How to break bad news. Baltimore, MD: John Hopkins University Press, 1992. Fallowfield L, et al. Communicating sad, bad, and difficult news in medicine. Lancet 2004; 363: 312–19. Kaye P. Breaking bad news: A ten step approach. Northampton: EPL Publications, 1996.

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4 Referral to the coroner It is not uncommon to be required to discuss the deaths of critically ill patients with a member of the coroner’s office, or to the procurator fiscal in Scotland The role of the coroner is to investigate deaths that are unexpected, unexplained, violent or unnatural, occur whilst in custody, or occur as the result of a medical mishap. The coroner is tasked with establishing who the deceased was, as well as where, when, and how they died.

Deaths requiring referral to the coroner • Where the cause is unknown or unclear. • Any sudden or unexpected death, including: • Sudden infant death • Stillbirths where there was a possibility of the child being born alive • Any death which is ‘unnatural’, including: • Deaths associated with poisoning (deliberate or accidental) • Death associated with therapeutic or recreational drug usage, including alcohol overdose • Death which may be related to an accident • Any death which may be related to industrial disease. • Any death associated with violence, including: • Death connected with a crime, or suspected crime • Suspected suicide • Any death associated with neglect, including: • Self-neglect, including chronic alcoholism • Neglect by others • If the deceased was not seen professionally by a doctor during their last illness, within 14 days of death (28 days in Northern Ireland), or after death. • Death occurring during an operation, or before recovery from an anaesthetic. • Any death in custody or detention, or occurring shortly after release. Referral inclusion criteria are deliberately broad, and in practice the list should be interpreted as including any unexpected hospital death, death from a complication of routine treatment, or trauma-related death. After discussion, the coroner may ask whether or not, as the reporting medical practitioner, you are able to issue a death certificate (e.g. where potentially life-saving surgery has been attempted in an otherwise dying individual). Alternatively (or in cases where you are not able to issue a death certificate), the coroner will take over the case. The coroner may require a postmortem examination in order to ascertain the cause of death (this cannot be refused), and may hold an inquest (or fatal accident inquiry in Scotland), for which you may be required to write a factual report and/or attend and give evidence.

REFERRAL TO THE CORONER

Verdicts (or Findings, Northern Ireland, or Determinations, Scotland) may be narrative in form, analysing the context and causes of the death. Alternatively ‘short form’ verdicts may be used, of which the commonest are: • Natural causes. • Accidental death, or death by misadventure. • Suicide. • Unlawful or lawful killing. • Industrial disease. • Open verdicts (there is insufficient evidence for any other verdict). Coroners are independent of government, and are not part of the civil or criminal courts. The coroner does not attribute culpability or liability. The coroner can, however, draw the case to the attention of an appropriate authority (for instance, if a further death could be prevented).

Pitfalls/difficult situations • Organ donation may still be possible in brain-dead individuals or potential ‘non-heart beating donors’ who require referral to the coroner; contact the coroner, who may allow donation to go ahead. • There are no time limits as to when a death may be attributable to a violent or medical cause. • The rules regarding what should be reported to the procurator fiscal in Scotland are essentially the same as those in England and Wales, but a previous publication includes a list which is much more specific in certain areas: • Possible or suspected suicide • Accidents: any death arising from the use of a vehicle including an aircraft, a ship, or a train; any death by drowning; any death by burning or scalding or as a result of a fire or explosion • Certain deaths of children: any death of a newborn child whose body is found, any death from apparent sudden infant death syndrome (cot death), any death of a child from suffocation including overlaying, any death of a foster child • Occupational: any death at work, whether or not as a result of an accident; any death related to occupation, e.g. industrial disease or poisoning • Any death following an abortion or attempted abortion • Any death as a result of a medical mishap, and any death where a complaint is received which suggests that medical treatment or the absence of treatment may have contributed to the death • Any death due to notifiable infectious disease, or food poisoning • Any death of a person of residence unknown, who died other than in a house

Further reading Crown Office. Death and the procurator fiscal. London: Crown Office Publication, November 1998. Crown Office and Procurator Fiscal Service. The role of the procurator fiscal in the investigation of deaths. London: Crown Office and Procurator Fiscal Service, 2009. General Medical Council. Treatment and care towards the end of life. London: GMC, 2010. Ministry of Justice. A guide to coroners and inquests. London: Ministry of Justice 2010.

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3 The potential organ donor Patients may be considered for organ donation after brainstem death or after cardiac death (‘non-heart-beating donors’).

Brainstem death Two doctors (one a consultant) are required to perform brainstem death tests. Both must be competent to perform the tests and be registered with the GMC for 5 years. Neither may be connected with transplant team. Two sets of tests are required with a gap in between (there is no set time period). Both doctors should be present at both tests. Death is confirmed after the 2nd set of tests, but time of death is after the 1st test.

Criteria for brainstem death Exclusions • Is the core temperature 6.65 kPa with a pH